Clinical Focus

  • Urology

Academic Appointments

Administrative Appointments

  • Member, Education Committee, International Continence Society (2016 - Present)

Honors & Awards

  • Basic Science Poster Award (Poster #BS20 Intradetrusor iPSC pSMC Treatment Rat Radiation Cystitis), SUFU 2019 Annual Meeting, Miami, FL (2019 (02/26))
  • 3rd Place in Category Prize (Poster Session 1 #15 Targeting Bladder Trigone in Cadaver), WSAUA 2018 Annual Meeting, Maui, HI (2018 (10/28))
  • Visiting Lecture (Management of Acute and Late Stage Complications of Radiation on Bladder), Cancer Diagnosis and Treatment Peak Forum, Tongji Medical College, Wuhan, Hubei, China (2018 (10/13))
  • Best in Category Prize (S23 Podium #443 Large Capacity Bladder after Prolapse Repair), ICS 2018 Annual Meeting, Philadelphia, PA (2018 (08/30))
  • Best Poster (MP33-12 Voiding Efficiency Following Correction Bladder Outlet Obstruction in Women), AUA 2018 Annual Meeting, San Francisco, CA. (2018 (05/19))
  • Early-Career Investigators Showcase (Pelvic Irradiation Induces Two Phenotypes - OAB vs UAB), AUA 2018 Annual Meeting, San Francisco, CA. (2018 (05/19))
  • Research Travel Award (Radiation Induced Bladder Dysfunction in the Rat), Basic Sciences Symposium. AUA 2017 Annual Meeting. Boston, MA. (2017 (05/12))
  • Best Clinical Research Award (Isometric Detrusor Reserve Predicts Spontaneous Void after TURP), Congress of Urologic Research and Education on Aging Underactive Bladder (CURE-UAB), Washington D.C. (2017 (03/09))
  • Travel Scholarship. CURE-UAB 2017 Meeting., Congress of Urologic Research and Education on Aging Underactive Bladder (CURE-UAB), Washington D.C. (2017 (03/09))
  • Spectrum KL2 Scholar, Stanford Clinical and Translational Science Award (2016-2018), Stanford University School of Medicine, Stanford, CA (2016 (07/01))
  • Best Resident Research Award (2014 - 2015), Albany Medical Center, Div. of Urology, Albany, NY (2015 (06/19))
  • 1st Place National Chief Resident Debate (Bladder Exstrophy: Argument for Modern Staged Repair), American Urological Association, 2015 Annual Meeting, New Orleans, LA (2015 (05/17))
  • Best Resident Teaching Award (2013 - 2014), Albany Medical Center, Div. of Urology, Albany, NY (2014 (06/20))
  • 2nd Place Resident Debate (Orchiopexy Retractile Testicle: Argument for Surgery), Northeast Section American Urological Association, 65th Annual Meeting, Saratoga Springs, NY (2013 (11/02))
  • 2nd Place Prize Essay Contest (Model of pelvic floor dysfunction after pelvic floor stimulation), Northeast Section American Urological Association, 65th Annual Meeting, Saratoga Springs, NY (2013 (11/01))
  • Best Resident Research Award (2012 - 2013), Albany Medical Center, Div. of Urology, Albany, NY (2013 (06/21))
  • 3rd Place Basic Science Competition (Loss renal protein phosphatase obstructive uropathy), 18th Annual Urology Resident Research Day, Skaneateles, NY (2013 (04/20))
  • 1st Place Prize Essay Contest (PPM1A and TGF-beta/SMAD signalling obstructive uropathy), Northeast Section American Urological Association, 64th Annual Meeting, Niagara Falls, Ontario (2012 (09/14))
  • 1st Place Resident Debate (Acute versus Delayed Prosthesis after Priapism), 17th Annual Urology Resident Research Day, Skaneateles, NY (2012 (04/21))

Boards, Advisory Committees, Professional Organizations

  • Member, Western Section American Urological Association (2018 - Present)
  • Member, American Urological Association (2011 - Present)
  • Member, Society of Women in Urology (2011 - Present)
  • Member, GLMA (2014 - Present)
  • Member, WPATH (2015 - Present)
  • Member, International Continence Society (2016 - Present)
  • Education Committee, International Continence Society (2016 - Present)

Professional Education

  • Master of Science, Stanford University Division of Epidemiology (2018)
  • Fellowship:Stanford University Dept of Urology (2017) CA
  • Residency:Albany Medical College Urologic Surgery Residency (2015) NY
  • Residency:Albany Medical College General Surgery Residency (2011) NY
  • Medical Education:University of North Carolina School of Medicine (2010) NC
  • Bachelor of Science, North Carolina State University (2004)

Research & Scholarship

Current Research and Scholarly Interests

Dr. Amy Dobberfuhl, received a B.S. in Mechanical Engineering from North Carolina State University in 2004 and her M.D. from the University of North Carolina at Chapel Hill School of Medicine in 2010. She completed her residency training in Urology at Albany Medical College in New York in 2015. She then completed an ACGME fellowship in FPMRS (Neurourology & Voiding Dysfunction) in the Department of Urology at Stanford University in 2017, and completed her M.S. in Epidemiology and Clinical Research from Stanford University in 2018. Following fellowship Dr. Dobberfuhl was appointed the faculty research position of Instructor in the Department of Urology 7/1/2017 and her practice includes both a clinical and research focus.

Dr. Dobberfuhl's current clinical practice includes: Pelvic Reconstruction, Neurourology, and Voiding Dysfunction.

Dr. Dobberfuhl?s current research focus includes: basic science, clinical and translational research in overactive / underactive bladder and radiation cystitis; urine biomarkers of compensated and decompensated detrusor dysfunction; animal models of voiding and pelvic floor dysfunction; pharmacologic modulation of lower urinary tract function and fibrosis. Dr. Dobberfuhl?s past basic science and clinical research interests have included: animal models of voiding and pelvic floor dysfunction (mouse, rat, rabbit); renal fibrosis and molecular cell signaling inflammatory pathways; pelvic floor ischemia; neuroanatomy and bladder tissue mechanics.

Dr. Dobberfuhl's basic science and clinical translational research efforts for 2016-2018 were supported by the Stanford Clinical and Translation Science Award to Spectrum (NIH KL2 TR 001083). To complement her KL2 sponsored research activities and translational research goals, she obtained an M.S. in Epidemiology and Clinical Research. Recent projects have included a CIRM grant (PI: Bertha Chen, MD), to investigate a novel iPSC pSMC stem cell therapy for the treatment of radiation cystitis; "Prevention of the Late Stage Adverse Effects of Radiation on the Bladder using Human Induced Pluripotent Stem Cells in a Rat Model of Radiation Cystitis". Through a SUFU grant, Dr. Dobberfuhl's research has explored the physiologic effect of the various onabotulinumtoxinA chemodenervation injection patterns in use today, project titled "Localization of OnabotulinumtoxinA and Cystometric Response Following Single versus Multiple Injections for the Treatment of Overactive Bladder in a Rat Model". Upcoming activities include a patient oriented research proposal to investigate the basic science mechanisms of underactive bladder and the creation of a benign urologic urine bio-repository for the identification of urine biomarkers of compensated and decompensated detrusor dysfunction. In collaboration with her basic science colleagues Dr. Bertha Chen (Urogynecology) and Dr. Edward Diaz (Pediatric Urology), Dr. Dobberfuhl's additional laboratory activities include exploring novel pharmacologic targets which may modulate lower urinary tract function and fibrosis. Currently funded projects and collaborators include the following:

1. WSDM Grant (PD/Co-PI Amy Dobberfuhl, Co-PI Elizabeth Kidd, Co-I Bertha Chen): ?Sex Differences in Lower Urinary Tract Function after Pelvic Radiation?
2. M.S. Epi-CR / Spectrum KL2 (PI/PD Amy Dobberfuhl, Co-I Steven Goodman, Bertha Chen) "Correction of Partial Bladder Outlet Obstruction in Women with Prolapse (2009-2015)"
3. SUFU Grant (Fellow PI Raveen Syan, Faculty PI Amy Dobberfuhl, Co-I Craig Comiter): ?Transvaginal OnabotulinumtoxinA Chemodenervation of the Trigone for the Third Line Treatment of Overactive Bladder?
4. SUFU Grant (Fellow PI Shannon Wallace, Faculty PI Bertha Chen, Faculty co-I Amy Dobberfuhl): ?Optogenetic Neuromodulation in of Diabetic Cystopathy?
5. CIRM Grant (PI/PD Bertha Chen, Co-I Amy Dobberfuhl): ?Human Induced Pluripotent Stem Cells in a Rat Model of Radiation Cystitis"


Graduate and Fellowship Programs


All Publications

  • Spontaneous voiding is surprisingly recoverable via outlet procedure in men with underactive bladder and documented detrusor underactivity on urodynamics. Neurourology and urodynamics Dobberfuhl, A. D., Chen, A., Alkaram, A. F., De, E. J. 2019


    AIMS: To identify clinical and urodynamic factors leading to spontaneous voiding in men with detrusor underactivity (DU) and suspected bladder outlet obstruction who underwent an outlet de-obstruction procedure.METHODS: We identified 614 men who underwent an outlet procedure at our institution from 2005 to 2014. Men were stratified by bladder contractility index (BCI). The primary outcome was spontaneous voiding after surgery. Data were analyzed in Statistical analysis system software.RESULTS: Of the 131 men who underwent preoperative urodynamics, 122 (mean age 68 years) had tracings available for review. DU (BCI<100) was identified in 54% (66 of 122), of whom only 68% (45 of 66) voided spontaneously before surgery, compared with 82% (46 of 56) of men with BCI?100. At a mean follow-up of 6.4 months postoperatively, 79% (52 of 66) of men with DU were able to void spontaneously, compared with 96% (54 of 56) of men with BCI?100. In men with a BCI<100 unable to void before surgery, 57% (12 of 21) recovered spontaneous voiding after surgery. On logistic regression for the outcome postoperative spontaneous voiding, significant preoperative characteristics, and urodynamic factors included preoperative spontaneous voiding (odds ratio [OR]=9.460; 95% confidence interval [CI]=2.955-30.289), increased maximum flow rate (Qmax; OR=1.184; 95% CI=1.014-1.382), increased detrusor pressure at maximum flow (Pdet@Qmax; OR=1.032; 95% CI=1.012-1.052), DU with BCI<100 (OR=0.138; 95% CI=0.030-0.635), and obstruction with bladder outlet obstruction index>40 (OR=5.595; 95% CI=1.685-18.575).CONCLUSION: Outlet de-obstruction improves spontaneous voiding in men with DU and may benefit men who do not meet the urodynamic threshold for obstruction.

    View details for DOI 10.1002/nau.24122

    View details for PubMedID 31432550

  • Evaluation and treatment of female stress urinary incontinence after pelvic radiotherapy NEUROUROLOGY AND URODYNAMICS Dobberfuhl, A. D. 2019; 38: S59?S69

    View details for DOI 10.1002/nau.23839

    View details for Web of Science ID 000481897500008

  • Urodynamic factors associated with the large capacity bladder and incomplete emptying after prolapse repair (2009-2015) NEUROUROLOGY AND URODYNAMICS Dobberfuhl, A. D., Shaffer, R. K., Goodman, S. N., Chen, B. H. 2019; 38 (5): 1322?31

    View details for DOI 10.1002/nau.23982

    View details for Web of Science ID 000471901900016

  • Are Fibroid and Bony Pelvis Characteristics Associated with Urinary and Pelvic Symptom Severity? American journal of obstetrics and gynecology Shaffer, R. K., Dobberfuhl, A. D., Vu, K., Fast, A. M., Dababou, S., Marrocchio, C., Lum, D. A., Hovsepian, D. M., Ghanouni, P., Chen, B. 2019


    BACKGROUND: Urinary and pelvic floor symptoms are often attributed to size and location of uterine fibroids. However, direct supporting evidence linking increased size to worsening symptoms is scant and limited to ultrasound evaluation of fibroids. Because management of fibroids is targeted towards symptomatic relief, identification of fibroid and pelvic characteristics associated with worse symptoms is vital to optimizing therapies and preventing needless interventions.OBJECTIVES: We examined the correlation between urinary, pelvic floor and fibroid symptoms, and fibroid size and location using precise uterine fibroid and bony pelvis characteristics obtained from magnetic resonance imaging (MRI).STUDY DESIGN: A retrospective review (2013-2017) of a multidisciplinary fibroid clinic identified 338 women examined via pelvic MRI, Pelvic Floor Distress Inventory questionnaire (PFDI; score 0-300), and a Uterine Fibroid Symptoms questionnaire (UFS; score 1-100). Multiple linear regression analysis was used to assess the influence of clinical factors and MRI findings on scaled PFDI and UFS scores. Data were analyzed in STATA.RESULTS: Our cohort of 338 women had a median PFDI of 72.7 (IQR 41-112.3). Increased PFDI score was associated with clinical factors of higher BMI (p<0.001), non-commercial insurance (p<0.001), increased parity (p=0.001) and history of incontinence surgery (p=0.003). Uterine volume, dominant fibroid volume, dimension and location, and fibroid location relative to the bony pelvis structure did not reach significance when compared with pelvic floor symptom severity. The mean UFS score was 52.0 (SD 23.5). Increased UFS score was associated with dominant submucosal fibroid (p=0.011) as well as BMI (p<0.0016), and a clinical history of anemia (p<0.001) or any hormonal treatment for fibroids (p=0.009).CONCLUSION: Contrary to common belief, in this cohort of women presenting for fibroid care, size and position of fibroids or uterus were not associated with pelvic floor symptom severity. Whereas, bleeding symptom severity was associated with dominant submucosal fibroid and prior hormonal treatment. Careful attention to clinical factors such as BMI and medical history is recommended when evaluating pelvic floor symptoms in women with uterine fibroids.

    View details for PubMedID 30711512

  • Transvaginal ultrasound guided trigone and bladder injection: A cadaveric feasibility study for a novel route of intradetrusor chemodenervation INVESTIGATIVE AND CLINICAL UROLOGY Syan, R., Briggs, M. A., Olivas, J. C., Srivastava, S., Comiter, C., Dobberfuhl, A. D. 2019; 60 (1): 40?45


    OnabotulinumtoxinA (BTX) detrusor chemodenervation is an efficacious third-line treatment for overactive bladder. Despite high clinical efficacy rates for BTX injection, many patients refuse initial or repeat treatment due to the invasiveness of the cystoscopic route of delivery. We assess the feasibility of injecting the trigone and posterior bladder wall via a transvaginal route under ultrasound guidance using a human cadaveric model.Eight de-identified anonymous fresh female deceased donor cadaver pelvises were placed in supine split leg position. A transvaginal ultrasound probe guided injections of India ink into the trigone in 3 sites and the posterior wall in 2 sites. Full thickness bladder biopsies were then obtained and histologic analysis was performed to confirm presence of India ink in the detrusor layer.The mean time from day of death was 11.0 days (range, 4.0-23.0 days). Three to five bladder biopsies were obtained per cadaver, for a total of 34 specimens (20 trigone, 14 posterior wall). Histologic analysis revealed presence of India ink within the detrusor layer in 8/8 (100.0%) of cadavers. The surgeon's perception of appropriate targeting under ultrasound guidance was confirmed in 8/8 cadavers (100.0%) involving the bladder trigone, and 7/8 (87.5%) involving the posterior wall. Of injections that were believed to have appropriately targeted the detrusor layer, 22/34 specimens (64.7%) demonstrated the presence of India ink under histologic analysis.Intradetrusor injection of the bladder trigone and posterior wall under transvaginal ultrasound guidance is feasible and has acceptable accuracy.

    View details for PubMedID 30637360

    View details for PubMedCentralID PMC6318206

  • Evaluation and treatment of female stress urinary incontinence after pelvic radiotherapy. Neurourology and urodynamics Dobberfuhl, A. D. 2018


    INTRODUCTION: Pelvic radiotherapy is associated with both acute and chronic voiding dysfunction. A review of the success and complications of surgical treatments for female stress urinary incontinence after pelvic radiotherapy has not been summarized in the published literature.METHODS: A systematic review of female stress urinary incontinence after pelvic radiotherapy was conducted using MeSH terminology (1988-2018).RESULTS: There is limited published literature on the treatment of stress urinary incontinence in women following pelvic radiotherapy. Long term indwelling urethral catheter should be avoided in all women given the risk of iatrogenic hypospadias. Surgical treatments can be classified into those for the intact versus failed outlet. Urethral bulking injections have been studied in a prospective fashion specifically in women with stress urinary incontinence after radiotherapy and although not randomized, have the highest level of evidence. Patients should be screened for a history of prior radiotherapy before considering sling placement. Artificial urinary sphincter is associated with a high rate of erosion after prior radiotherapy. The role of Burch colposuspension in patients with prior radiotherapy is poorly defined. Urinary diversion should be considered for patients with a devastated outlet.CONCLUSIONS: Since the long-term effects of radiotherapy on lower urinary tract voiding function are typically irreversible and progressive, further research is needed to mitigate the adverse effects of irradiation and identify more durable treatment options for women with radiation induced bladder dysfunction and stress urinary incontinence.

    View details for PubMedID 30311659

  • Peroxisome proliferator-activated receptor gamma agonist as a novel treatment for interstitial cystitis: A rat model INVESTIGATIVE AND CLINICAL UROLOGY Mahal, A., Young-Lin, N., Dobberfuhl, A., Estes, J., Comiter, C. 2018; 59 (4): 257?62
  • Peroxisome proliferator-activated receptor gamma agonist as a novel treatment for interstitial cystitis: A rat model. Investigative and clinical urology Mahal, A., Young-Lin, N., Dobberfuhl, A., Estes, J., Comiter, C. V. 2018; 59 (4): 257?62


    Purpose: To understand the therapeutic potential of pioglitazone, a peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist with a propensity to cause bladder mucosal proliferation, on interstitial cystitis (IC) in a rat model.Materials and Methods: Using a previously described animal model for IC, Sprague-Dawley rats were treated with biweekly cyclophosphamide injections (35 mg/kg) to induce cystitis. Animals were divided into 4 groups (n=6 for each group): IC plus daily sham saline gavage (IC+Pio-), IC plus daily pioglitazone gavage (15 mg/kg) (IC+Pio+), normal rats with daily pioglitazone (IC-Pio+), and normal rats with neither IC nor pioglitazone (IC-Pio- or Control). At the end of four weeks, urinary frequency and bladder capacity were measured. Histologic examination of urothelial integrity was also performed.Results: Average voids per hour were significantly lower in IC+Pio+ (4.01.9) vs. IC+Pio- (10.02.4) rats (p<0.01) and were similar to IC-Pio+ (6.01.4) and IC-Pio- (6.01.5) controls. Cystometric capacity was significantly higher in IC+Pio+ (0.9450.122 mL) vs. IC+Pio- rats (0.5880.165 mL, p=0.01) and was comparable to IC-Pio- capacity (0.8170.196 mL) and IC-Pio+ capacity (0.9410.188 mL). Urothelial structural integrity was improved in IC+Pio+ rats versus IC+Pio- rats upon histologic observation.Conclusions: Pioglitazone, a PPAR-gamma agonist, improved bladder function in cyclophosphamide-induced cystitis by both observed urinary frequency and measured cystometric capacity. Urothelial structural integrity was also improved. Pioglitazone, due to a propensity to cause bladder mucosal proliferation, may prove useful for treating IC, and deserves further investigation.

    View details for PubMedID 29984341

  • Statewide Success of Staged Sacral Neuromodulation for the Treatment of Urinary Complaints in California (2005-2011) Female pelvic medicine & reconstructive surgery Dobberfuhl, A. D., Mahal, A., Dallas, K. B., Choi, K. M., Comiter, C. V., Elliott, C. S. 2018
  • A Systematic Approach to the Evaluation and Management of the Failed Artificial Urinary Sphincter. Current urology reports Dobberfuhl, A. D., Comiter, C. V. 2017; 18 (3): 18-?


    In men with post-prostatectomy incontinence, persistent or recurrent urinary leakage following artificial urinary sphincter placement is a frustrating complaint. Surgical failure can be classified as occurring early in the post-operative period vs. late-following a period of established continence-and should be managed according to the time course and severity of urinary leakage. We present a systematic approach for the evaluation and treatment of the failed artificial urinary sphincter. After considering the patient's individualized treatment goals and impact on quality of life, the clinician can more appropriately advise patients on a management strategy for their recurrent or persistent urinary incontinence following artificial urinary sphincter placement.

    View details for DOI 10.1007/s11934-017-0666-y

    View details for PubMedID 28233225

  • Chapter 9: Uterosacral Ligament Vaginal Vault Suspension Native Tissue Repair for Incontinence and Prolapse Dobberfuhl, A. D., De, E. J. Springer International Publishing. 2017: 131?142
  • Loss of expression of protein phosphatase magnesium-dependent 1A during kidney injury promotes fibrotic maladaptive repair FASEB JOURNAL Samarakoon, R., Rehfuss, A., Khakoo, N. S., Falke, L. L., Dobberfuhl, A. D., Helo, S., Overstreet, J. M., Goldschmeding, R., Higgins, P. J. 2016; 30 (10): 3308-3320


    Protein phosphatase magnesium-dependent-1A (PPM1A) dephosphorylates SMAD2/3, which suppresses TGF-? signaling in keratinocytes and during Xenopus development; however, potential involvement of PPM1A in chronic kidney disease is unknown. PPM1A expression was dramatically decreased in the tubulointerstitium in obstructive and aristolochic acid nephropathy, which correlates with progression of fibrotic disease. Stable silencing of PPM1A in human kidney-2 human renal epithelial cells increased SMAD3 phosphorylation, stimulated expression of fibrotic genes, induced dedifferentiation, and orchestrated epithelial cell-cycle arrest via SMAD3-mediated connective tissue growth factor and plasminogen activator inhibitor-1 up-regulation. PPM1A stable suppression in normal rat kidney-49 renal fibroblasts, in contrast, promoted a SMAD3-dependent connective tissue growth factor and plasminogen activator inhibitor-1-induced proliferative response. Paracrine factors secreted by PPM1A-depleted epithelial cells augmented fibroblast proliferation (>50%) compared with controls. PPM1A suppression in renal cells further enhanced TGF-?1-induced SMAD3 phosphorylation and fibrotic gene expression, whereas PPM1A overexpression inhibited both responses. Moreover, phosphate tensin homolog on chromosome 10 depletion in human kidney-2 cells resulted in loss of expression and decreased nuclear levels of PPM1A, which enhanced SMAD3-mediated fibrotic gene induction and growth arrest that were reversed by ectopic PPM1A expression. Thus, phosphate tensin homolog on chromosome 10 is an upstream regulator of renal PPM1A deregulation. These findings establish PPM1A as a novel repressor of the SMAD3 pathway in renal fibrosis and as a new therapeutic target in patients with chronic kidney disease.-Samarakoon, R., Rehfuss, A., Khakoo, N. S., Falke, L. L., Dobberfuhl, A. D., Helo, S., Overstreet, J. M., Goldschmeding, R., Higgins, P. J. Loss of expression of protein phosphatase magnesium-dependent 1A during kidney injury promotes fibrotic maladaptive repair.

    View details for DOI 10.1096/fj.201500105R

    View details for Web of Science ID 000384329800005

    View details for PubMedID 27328942

  • A Novel Cystometric Model of Pelvic Floor Dysfunction After Rabbit Pelvic Floor Noxious Electrical Stimulation FEMALE PELVIC MEDICINE AND RECONSTRUCTIVE SURGERY Dobberfuhl, A. D., Spettel, S., Schuler, C., Dubin, A. H., Levin, R. M., De, E. J. 2016; 22 (4): 248-253


    Although a relationship between pelvic floor dysfunction and lower urinary tract symptoms is described in the literature, the mechanism and pathways need further characterization. We developed an animal model of pelvic floor dysfunction after noxious stimulation of the pubococcygeus (PC) muscle.Fifteen female adult rabbits were evaluated with cystometry (CMG) and electromyography (EMG) recordings from the PC muscle. Cystometry/EMG was performed before and after treatment animal (n = 11) received noxious pelvic floor electrical stimulation through the PC EMG electrode, and controls (n = 4) underwent sham needle placement. Two animals underwent S3 dorsal rhizotomy to demonstrate that the observed results required afferent innervation.Voiding changes were demonstrated in 9 of 11 rabbits after stimulation. Most of the rabbits (7/9) exhibited a prolonged-dysfunctional voiding pattern with larger capacity (mean, 17 mL [SEM, 8 mL]), longer intercontractile interval (227% [SEM, 76%]) and duration (163% [SEM, 20%]), and increased postvoid residual (24 mL [SEM, 6 mL]). The remaining dysfunctional rabbits (2/9) exhibited an overactive-dysfunctional voiding pattern with lower capacity (-26 mL [SEM, 6 mL]), shortened intercontractile interval (16% [SEM, 9%]) and duration (56% [SEM, 30%]), and decreased postvoid residual (-27 mL [SEM, 6 mL]). Nonresponder rabbits (2/11) were relatively unchanged in their micturition cycles after stimulation. Rhizotomy animals were acontractile and filled until overflow incontinence occurred.Using noxious electrical stimulation of the pelvic musculature, we were able to produce an animal model of pelvic floor dysfunction in most rabbits as hallmarked by a larger bladder capacity, an increased intercontractile interval, and prolonged contraction duration.

    View details for DOI 10.1097/SPV.0000000000000253

    View details for Web of Science ID 000378713200013

    View details for PubMedID 26829345

  • The artificial urinary sphincter and male sling for postprostatectomy incontinence: Which patient should get which procedure? Investigative and clinical urology Comiter, C. V., Dobberfuhl, A. D. 2016; 57 (1): 3-13


    Surgery is the most efficacious treatment for postprostatectomy incontinence. The ideal surgical approach depends on a variety of patient factors including history of prior incontinence surgery or radiation treatment, bladder contractility, severity of leakage, and patient expectations. Most patients choose to avoid a mechanical device, opting for the male sling over the artificial urinary sphincter. The modern male sling has continued to evolve with respect to device design and surgical technique. Various types of slings address sphincteric incompetence via different mechanisms of action. The recommended surgery, however, must be individualized to the patient based on degree of incontinence, detrusor contractility, and urethral compliance. A thorough urodynamic evaluation is indicated for the majority of patients, and the recommendation for an artificial urinary sphincter, a transobturator sling, or a quadratic sling will depend on urodynamic findings and the patient's particular preference. As advancements in this field evolve, and our understanding of the pathophysiology of incontinence and mechanisms of various devices improves, we expect to see continued evolution in device design.

    View details for DOI 10.4111/icu.2016.57.1.3

    View details for PubMedID 26966721

    View details for PubMedCentralID PMC4778750

  • Initial Evaluation and Management of Acute Urinary Retention AUA Update Series Dobberfuhl, A. D., Comiter, C. V. 2016; 35: 95-104
  • Noxious electrical stimulation of the pelvic floor and vagina induces transient voiding dysfunction in a rabbit survival model of pelvic floor dystonia. Korean journal of urology Dobberfuhl, A. D., Spettel, S., Schuler, C., Levin, R. M., Dubin, A. H., De, E. J. 2015; 56 (12): 837-844


    Existing data supports a relationship between pelvic floor dysfunction and lower urinary tract symptoms. We developed a survival model of pelvic floor dysfunction in the rabbit and evaluated cystometric (CMG), electromyographic (EMG) and ambulatory voiding behavior.Twelve female adult virgin rabbits were housed in metabolic cages to record voiding and defecation. Anesthetized CMG/EMG was performed before and after treatment animals (n=9) received bilateral tetanizing needle stimulation to the pubococcygeous (PC) muscle and controls (n=3) sham needle placement. After 7 days all animals were subjected to tetanizing transvaginal stimulation and CMG/EMG. After 5 days a final CMG/EMG was performed.Of rabbits that underwent needle stimulation 7 of 9 (78%) demonstrated dysfunctional CMG micturition contractions versus 6 of 12 (50%) after transvaginal stimulation. Needle stimulation of the PC musculature resulted in significant changes in: basal CMG pressure, precontraction pressure change, contraction pressure, interval between contractions and postvoid residual; with time to 3rd contraction increased from 38 to 53 minutes (p=0.008 vs. prestimulation). Vaginal noxious stimulation resulted in significant changes in: basal CMG pressure and interval between contractions; with time to 3rd contraction increased from 37 to 46 minutes (p=0.008 vs. prestimulation). Changes in cage parameters were primarily seen after direct needle stimulation.In a majority of animals, tetanizing electrical stimulation of the rabbit pelvic floor resulted in voiding changes suggestive of pelvic floor dysfunction as characterized by a larger bladder capacity, longer interval between contractions and prolonged contraction duration.

    View details for DOI 10.4111/kju.2015.56.12.837

    View details for PubMedID 26682025

    View details for PubMedCentralID PMC4681762

  • Female stress urinary incontinence and the mid-urethral sling: Is obstruction necessary to achieve dryness? WORLD JOURNAL OF UROLOGY Dobberfuhl, A. D., De, E. J. 2015; 33 (9): 1243-1250


    Recently, the American Urogynecologic Society and Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction released position statements on the use of mid-urethral slings. The statement offers that the polypropylene mesh mid-urethral sling (retropubic and transobturator) is now the recognized worldwide standard of care for the surgical treatment of stress urinary incontinence. The purpose of the current manuscript is to examine whether the polypropylene mesh mid-urethral sling should be the standard of care.Data for this review were acquired by a systematic search of the medical literature.The Trial of Mid-Urethral Slings found that retropubic and transobturator slings were associated with a significant rate of adverse events, despite being comprised of surgeons from high-volume, experienced centers. Stress urinary incontinence is not just a urethral disease due to intrinsic sphincteric deficiency. It can also be related to urethral hypermobility, which in turn is caused by anterior vaginal wall laxity. Often both hypermobility and intrinsic sphincter deficiency coexist. Recognizing the role of anterior vaginal wall support is important to understanding the role of procedures (such as Burch or needle suspension procedures) which have the potential of correcting stress incontinence without affecting voiding parameters.As a discipline, we need to conceptualize stress incontinence due to urethral hypermobility or intrinsic sphincter deficiency as separate entities and design our procedures to restore the underlying suspected pathology.

    View details for DOI 10.1007/s00345-015-1600-x

    View details for Web of Science ID 000360509100005

    View details for PubMedID 26025190

  • Loss of tumour suppressor PTEN expression in renal injury initiates SMAD3-and p53-dependent fibrotic responses JOURNAL OF PATHOLOGY Samarakoon, R., Helo, S., Dobberfuhl, A. D., Khakoo, N. S., Falke, L., Overstreet, J. M., Goldschmeding, R., Higgins, P. J. 2015; 236 (4): 421-432


    Deregulation of the tumour suppressor PTEN occurs in lung and skin fibrosis and diabetic and ischaemic renal injury. However, the potential role of PTEN and associated mechanisms in the progression of kidney fibrosis is unknown. Tubular and interstitial PTEN expression was dramatically decreased in several models of renal injury, including aristolochic acid nephropathy (AAN), streptozotocin (STZ)-mediated injury and ureteral unilateral obstruction (UUO), correlating with Akt, p53 and SMAD3 activation and fibrosis. Stable silencing of PTEN in HK-2 human tubular epithelial cells induced dedifferentiation and CTGF, PAI-1, vimentin, ?-SMA and fibronectin expression, compared to HK-2 cells expressing control shRNA. Furthermore, PTEN knockdown stimulated Akt, SMAD3 and p53(Ser15) phosphorylation, with an accompanying decrease in population density and an increase in epithelial G1 cell cycle arrest. SMAD3 or p53 gene silencing or pharmacological blockade partially suppressed fibrotic gene expression and relieved growth inhibition orchestrated by deficiency or inhibition of PTEN. Similarly, shRNA suppression of PAI-1 rescued the PTEN loss-associated epithelial proliferative arrest. Moreover, TGF?1-initiated fibrotic gene expression is further enhanced by PTEN depletion. Combined TGF?1 treatment and PTEN silencing potentiated epithelial cell death via p53-dependent pathways. Thus, PTEN loss initiates tubular dysfunction via SMAD3- and p53-mediated fibrotic gene induction, with accompanying PAI-1-dependent proliferative arrest, and cooperates with TGF?1 to induce the expression of profibrotic genes and tubular apoptosis.

    View details for DOI 10.1002/path.4538

    View details for Web of Science ID 000358302900004

    View details for PubMedID 25810340

  • Identification of CNS Neurons Innervating the Levator Ani and Ventral Bulbospongiosus Muscles in Male Rats JOURNAL OF SEXUAL MEDICINE Dobberfuhl, A. D., Oti, T., Sakamoto, H., Marson, L. 2014; 11 (3): 664-677


    The pelvic striated muscles play an important role in mediating erections and ejaculation, and together these muscles compose a tightly coordinated neuromuscular system that is androgen sensitive and sexually dimorphic.To identify spinal and brains neurons involved in the control of the levator ani (LA) and bulbospongiosus (BS) in the male adult and preadolescent rat.Rats were anesthetized, and the transsynaptic retrograde tracer pseudorabies virus (PRV) was injected into the LA muscle of adults or the ventral BS muscle in 30-day-old rats. After 3-5 days rats were sacrificed, and PRV-labeled neurons in the spinal cords and brains were identified using immunohistochemistry. The presence of gastrin-releasing peptide (GRP) in the lumbar spinal neurons was examined.The location and number of PRV-labeled neurons in the spinal cord and brain and GRP colocalization in the lumbar spinal cord.PRV-labeled spinal interneurons were found distributed throughout T11-S1 of the spinal cord, subsequent to dorsal medial motoneuron infection. The majority of spinal interneurons were found in the lumbosacral spinal cord in the region of the dorsal gray commissure and parasympathetic preganglionic neurons. Preadolescent rats had more PRV-labeled spinal interneurons at L5-S1 where the motoneurons were located but relatively less spread rostrally in the spinal cord compared with adults. Lumbar spinothalmic neurons in medial gray of L3-L4 co-localized PRV and GRP. In the brain consistent labeling was seen in areas known to be involved in male sexual behavior including the ventrolateral medulla, hypothalamic paraventricular nucleus, and medial preoptic area.Common spinal and brain pathways project to the LA and BS muscles in the rat suggesting that these muscles act together to coordinate male sexual reflexes. Differences may exist in the amount of synaptic connections/neuronal pathways in adolescents compared with adults.

    View details for DOI 10.1111/jsm.12418

    View details for Web of Science ID 000332140300006

    View details for PubMedID 24373488

  • Evaluation & Treatment of Overactive Bladder AUA University: Core Curriculum Dobberfuhl, A. D., De, E. J. American Urological Association. 2014
  • Induction of renal fibrotic genes by TGF-beta 1 requires EGFR activation, p53 and reactive oxygen species CELLULAR SIGNALLING Samarakoon, R., Dobberfuhl, A. D., Cooley, C., Overstreet, J. M., Patel, S., Goldschmeding, R., Meldrum, K. K., Higgins, P. J. 2013; 25 (11): 2198-2209


    While transforming growth factor-? (TGF-?1)-induced SMAD2/3 signaling is a critical event in the progression of chronic kidney disease, the role of non-SMAD mechanisms in the orchestration of fibrotic gene changes remains largely unexplored. TGF-?1/SMAD3 pathway activation in renal fibrosis (induced by ureteral ligation) correlated with epidermal growth factor receptor(Y845) (EGFR(Y845)) and p53(Ser15) phosphorylation and induction of disease causative target genes plasminogen activator inhibitor-1 (PAI-1) and connective tissue growth factor (CTGF) prompting an investigation of the mechanistic involvement of EGFR and tumor suppressor p53 in profibrotic signaling. TGF-?1, PAI-1, CTGF, p53 and EGFR were co-expressed in the obstructed kidney localizing predominantly to the tubular and interstitial compartments. Indeed, TGF-?1 activated EGFR and p53 as well as SMAD2/3. Genetic deficiency of either EGFR or p53 or functional blockade with AG1478 or Pifithrin-?, respectively, effectively inhibited PAI-1and CTGF induction and morphological transformation of renal fibroblasts as did SMAD3 knockdown or pretreatment with the SMAD3 inhibitor SIS3. Reactive oxygen species (ROS)-dependent mechanisms initiated by TGF-?1 were critical for EGFR(Y845) and p53(Ser15) phosphorylation and target gene expression. The p22(Phox) subunit of NADPH oxidase was also elevated in the fibrotic kidney with an expression pattern similar to p53 and EGFR. EGF stimulation alone initiated, albeit delayed, c-terminal SMAD3 phosphorylation (that required the TGF-?1 receptor) and rapid ERK2 activation both of which are necessary for PAI-1 and CTGF induction in renal fibroblasts. These data highlight the extensive cross-talk among SMAD2/3, EGFR and p53 pathways essential for expression of TGF-?1-induced fibrotic target genes.

    View details for DOI 10.1016/j.cellsig.2013.07.007

    View details for Web of Science ID 000324971800013

    View details for PubMedID 23872073

  • Ureteral Obstruction-Induced Renal Fibrosis: An In Vivo Platform for Mechanistic Discovery and Therapeutic Intervention. Cell & developmental biology Dobberfuhl, A. D., Samarakoon, R., Higgins, C. E., Mian, B. M., Overstreet, J. M., Higgins, S. P., Kogan, B. A., Higgins, P. J. 2012; 1 (3)

    View details for DOI 10.4172/2168-9296.1000e107

    View details for PubMedID 23264954

    View details for PubMedCentralID PMC3526117

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