Surgeons, Urologist


2705 Dekalb Pike
Ste 302
Norristown, PA 19401
610-277-0313
Locations and availability (4)

Affiliations ?

Dr. May is affiliated with 5 hospitals.

Hospital Affilations

Score

Rankings

  • Montgomery Hospital XXXXX
    900 E Fornance St, Norristown, PA 19401
    • Currently 3 of 4 crosses
    Top 50%
  • Albert Einstein Medical Center
    5501 Old York Rd, Philadelphia, PA 19141
    • Currently 3 of 4 crosses
    Top 50%
  • Germantown Hospital & Community Health Services
    1 Penn Blvd, Philadelphia, PA 19144
  • Elkins Park Hospital
    60 Township Line Rd, Elkins Park, PA 19027
  • Mossrehab & Albert Einstein Med Ctr
    60 Township Line Rd, Elkins Park, PA 19027
  • Publications & Research

    Dr. May has contributed to 9 publications.
    Title Serum Creatinine Predicts Success in Retrograde Ureteral Stent Placement in Patients with Pelvic Malignancies.
    Date September 2008
    Journal Urology
    Excerpt

    OBJECTIVES: To evaluate serum hemoglobin, baseline serum creatinine, serum creatinine at the diagnosis of obstructive hydronephrosis, and the increase in serum creatinine greater than baseline to predict for success in retrograde ureteral stent placement in patients with pelvic malignancies. METHODS: In a retrospective chart review, we identified 57 patients at our institution with obstructive hydronephrosis secondary to pelvic malignancies in which retrograde ureteral stent placement was attempted from January 2002 to May 2005. The patient charts were reviewed for the baseline serum creatinine, preoperative serum creatinine and hemoglobin, and serum creatinine at presentation of obstructive hydronephrosis. This population was divided into group 1 (n = 31, 54%), in which retrograde stent placement was successful, and group 2 (n = 26, 46%), in which stent placement failed and subsequent percutaneous nephrostomy tube placement was required. The Student t test was used to determine whether a significant difference existed between the two groups for each laboratory parameter. RESULTS: The serum hemoglobin and baseline creatinine were not significantly different between the two groups and could not be used to predict for the success or failure of stent placement (P = 0.10 and P = 0.59, respectively). However, the average serum creatinine at presentation of obstructive hydronephrosis was significantly different between group 1 (2.4 +/- 1.4 ng/dL) and group 2 (5.3 +/- 6.3; P = 0.014), as was an increase in serum creatinine greater than baseline (P = 0.002). CONCLUSIONS: The results of this study have shown that the serum creatinine level at the presentation of obstructive hydronephrosis can be used to predict for success in retrograde ureteral stent placement in patients with pelvic malignancies.

    Title Adjunctive Use of Androgel (testosterone Gel) with Sildenafil to Treat Erectile Dysfunction in Men with Acquired Androgen Deficiency Syndrome After Failure Using Sildenafil Alone.
    Date April 2006
    Journal Urology
    Excerpt

    OBJECTIVES: To evaluate whether combination therapy with testosterone gel (T-gel) and sildenafil citrate is effective in achieving adequate potency in subjects with low-normal serum testosterone levels in whom sildenafil alone has failed. METHODS: From July 2000 to June 2001, we evaluated 90 men (aged 32 to 72 years) in whom 3 months of sildenafil therapy at the maximal recommended dose (100 mg) with at least three attempts at intercourse during the 3-month period had failed. Of these, 24 men had testosterone levels less than 400 ng/dL (range 92 to 365, mean 231.4) and were subsequently started on 1% T-gel monotherapy (AndroGel, 5 g daily). After 4 weeks of T-gel alone (week 4), sildenafil citrate (Viagra, 100 mg) was added to the treatment regimen for an additional 12 weeks (through week 16). Potency was defined as the ability to have at least one episode of satisfactory intercourse during the treatment period. RESULTS: All the men had normalized serum testosterone levels after 4 weeks of T-gel monotherapy (range 424 to 596 ng/dL, mean 525). However, none of the men regained potency. At week 16, almost all (22 of 24, 92%) of the men reported improved potency with combination therapy. Improvement in erection quality was also observed. CONCLUSIONS: The results of this study support the use of T-gel with sildenafil citrate in men with low-normal serum testosterone levels in whom sildenafil alone fails. It also underscores the numbers of men with low to low-normal testosterone levels who would benefit from testosterone screening when evaluated for erectile dysfunction.

    Title Levels of the Origin-binding Protein Double Parked and Its Inhibitor Geminin Increase in Response to Replication Stress.
    Date January 2006
    Journal Journal of Cell Science
    Excerpt

    The regulation of a pre-replicative complex (pre-RC) at origins ensures that the genome is replicated only once per cell cycle. Cdt1 is an essential component of the pre-RC that is rapidly degraded at G1-S and also inhibited by Geminin (Gem) protein to prevent re-replication. We have previously shown that destruction of the Drosophila homolog of Cdt1, Double-parked (Dup), at G1-S is dependent upon cyclin-E/CDK2 and important to prevent re-replication and cell death. Dup is phosphorylated by cyclin-E/Cdk2, but this direct phosphorylation was not sufficient to explain the rapid destruction of Dup at G1-S. Here, we present evidence that it is DNA replication itself that triggers rapid Dup destruction. We find that a range of defects in DNA replication stabilize Dup protein and that this stabilization is not dependent on ATM/ATR checkpoint kinases. This response to replication stress was cell-type specific, with neuroblast stem cells of the larval brain having the largest increase in Dup protein. Defects at different steps in replication also increased Dup protein during an S-phase-like amplification cell cycle in the ovary, suggesting that Dup stabilization is sensitive to DNA replication and not an indirect consequence of a cell-cycle arrest. Finally, we find that cells with high levels of Dup also have elevated levels of Gem protein. We propose that, in cycling cells, Dup destruction is coupled to DNA replication and that increased levels of Gem balance elevated Dup levels to prevent pre-RC reformation when Dup degradation fails.

    Title Drosophila Double-parked is Sufficient to Induce Re-replication During Development and is Regulated by Cyclin E/cdk2.
    Date November 2004
    Journal Development (cambridge, England)
    Excerpt

    It is important that chromosomes are duplicated only once per cell cycle. Over-replication is prevented by multiple mechanisms that block the reformation of a pre-replicative complex (pre-RC) onto origins in S and G2 phase. We have investigated the developmental regulation of Double-parked (Dup) protein, the Drosophila ortholog of Cdt1, a conserved and essential pre-RC component found in human and other organisms. We find that phosphorylation and degradation of Dup protein at G1/S requires cyclin E/CDK2. The N terminus of Dup, which contains ten potential CDK phosphorylation sites, is necessary and sufficient for Dup degradation during S phase of mitotic cycles and endocycles. Mutation of these ten phosphorylation sites, however, only partially stabilizes the protein, suggesting that multiple mechanisms ensure Dup degradation. This regulation is important because increased Dup protein is sufficient to induce profound rereplication and death of developing cells. Mis-expression has different effects on genomic replication than on developmental amplification from chorion origins. The C terminus alone has no effect on genomic replication, but it is better than full-length protein at stimulating amplification. Mutation of the Dup CDK sites increases genomic re-replication, but is dominant negative for amplification. These two results suggest that phosphorylation regulates Dup activity differently during these developmentally specific types of DNA replication. Moreover, the ability of the CDK site mutant to rapidly inhibit BrdU incorporation suggests that Dup is required for fork elongation during amplification. In the context of findings from human and other cells, our results indicate that stringent regulation of Dup protein is critical to protect genome integrity.

    Title Transdifferentiation of the Ventral Retinal Pigmented Epithelium to Neural Retina in the Growth Arrest Specific Gene 1 Mutant.
    Date September 2001
    Journal Developmental Biology
    Excerpt

    During eye development, retinal pigmented epithelium (RPE) and neural retina (NR) arise from a common origin, the optic vesicle. One of the early distinctions of RPE from NR is the reduced mitotic activity of the RPE. Growth arrest specific gene 1 (Gas1) has been documented to inhibit cell cycle progression in vitro (G. Del Sal et al., 1992, Cell 70, 595--607). We show here that the expression pattern of Gas1 in the eye supports its negative role in RPE proliferation. To test this hypothesis, we generated a mouse carrying a targeted mutation in the Gas1 locus. Gas1 mutant mice have microphthalmia. Histological examination revealed that the remnant mutant eyes are ingressed from the surface with minimal RPE and lens, and disorganized eyelid, cornea, and NR. Analysis of the Gas1 mutant indicates that there is overproliferation of the outer layer of optic cup (E10.5) immediately after the initial specification of the RPE. This defect is specific to the ventral region of the RPE. Using molecular markers for RPE (Mi and Tyrp2) and NR (Math5), we demonstrate that there is a gradual loss of Mi and Tyrp2 expression and an appearance of Math5 expression in the mutant ventral RPE region, indicating that this domain becomes respecified to NR. This "ectopic" NR develops as a mirror image of the normal NR and is entirely of ventral identity. Our data not only support Gas1's function in regulating cell proliferation, but also uncover an unexpected regional-specific cell fate change associated with dysregulated growth. Furthermore, we provide evidence that the dorsal and ventral RPEs are maintained by distinct genetic components.

    Title Growth Arrest Specific Gene 1 is a Positive Growth Regulator for the Cerebellum.
    Date September 2001
    Journal Developmental Biology
    Excerpt

    Postnatal cerebellum development involves the generation of granule cells and Bergmann glias (BGs). The granule cell precursors are located in the external germinal layer (EGL) and the BG precursors are located in the Purkinje layer (PL). BGs extend their glial fibers into the EGL and facilitate granule cells' inward migration to their final location. Growth arrest specific gene 1 (Gas1) has been implicated in inhibiting cell-cycle progression in cell culture studies (G. Del Sal et al., 1992, Cell 70, 595--607). However, its growth regulatory function in the CNS has not been described. To investigate its role in cerebellar growth, we analyzed the Gas1 mutant mice. At birth, wild-type and mutant mice have cerebella of similar size; however, mature mutant cerebella are less than half the size of wild-type cerebella. Molecular and cellular examinations indicate that Gas1 mutant cerebella have a reduced number of granule cells and BG fibers. We provide direct evidence that Gas1 is required for normal levels of proliferation in the EGL and the PL, but not for their differentiation. Furthermore, we show that Gas1 is specifically and coordinately expressed in both the EGL and the BGs postnatally. These results support Gas1 as a common genetic component in coordinating EGL cell and BG cell proliferation, a link which has not been previously appreciated.

    Title Arnt2 Acts As the Dimerization Partner of Sim1 for the Development of the Hypothalamus.
    Date April 2000
    Journal Mechanisms of Development
    Excerpt

    One major function of the hypothalamus is to maintain homeostasis by modulating the secretion of pituitary hormones. The paraventricular (PVN) and supraoptic (SON) nuclei are major integration centers for the output of the hypothalamus to the pituitary. The bHLH-PAS transcription factor SIM1 is crucial for the development of several neuroendocrine lineages within the PVN and SON. bHLH-PAS proteins require heterodimerization for their function. ARNT, ARNT2, and BMAL1 are the three known general heterodimerization partners for bHLH-PAS proteins. Here, we provide evidence that Sim1 and Arnt2 form dimers in vitro, that they are co-expressed in the PVN and SON, and that their loss of function affects the development of the same sets of neuroendocrine cell types within the PVN and SON. Together, these results implicate ARNT2 as the in vivo dimerization partner of SIM1 in controlling the development of these neuroendocrine lineages.

    Title Shh-n Upregulates Sfrp2 to Mediate Its Competitive Interaction with Wnt1 and Wnt4 in the Somitic Mesoderm.
    Date March 2000
    Journal Development (cambridge, England)
    Excerpt

    Dorsoventral polarity of the somitic mesoderm is established by competitive signals originating from adjacent tissues. The ventrally located notochord provides the ventralizing signals to specify the sclerotome, while the dorsally located surface ectoderm and dorsal neural tube provide the dorsalizing signals to specify the dermomyotome. Noggin and SHH-N have been implicated as the ventralizing signals produced by the notochord. Members of the WNT family of proteins, on the other hand, have been implicated as the dorsalizing signals derived from the ectoderm and dorsal neural tube. When presomitic explants are confronted with cells secreting SHH-N and WNT1 simultaneously, competition to specify the sclerotome and dermomyotome domains within the naive mesoderm can be observed. Here, using these explant cultures, we provide evidence that SHH-N competes with WNT1, not only by upregulating its own receptor Ptc1, but also by upregulating Sfrp2 (Secreted frizzled-related protein 2), which encodes a potential WNT antagonist. Among the four known Sfrps, Sfrp2 is the only member expressed in the sclerotome and upregulated by SHH-N recombinant protein. We further show that SFRP2-expressing cells can reduce the dermomyotome-inducing activity of WNT1 and WNT4, but not that of WNT3a. Together, our results support the model that SHH-N at least in part employs SFRP2 to reduce WNT1/4 activity in the somitic mesoderm.

    Title Development of Neuroendocrine Lineages Requires the Bhlh-pas Transcription Factor Sim1.
    Date November 1998
    Journal Genes & Development
    Excerpt

    The bHLH-PAS transcription factor SIM1 is expressed during the development of the hypothalamic-pituitary axis in three hypothalamic nuclei: the paraventricular nucleus (PVN), the anterior periventricular nucleus (aPV), and the supraoptic nucleus (SON). To investigate Sim1 function in the hypothalamus, we produced mice carrying a null allele of Sim1 by gene targeting. Homozygous mutant mice die shortly after birth. Histological analysis shows that the PVN and the SON of these mice are hypocellular. At least five distinct types of secretory neurons, identified by the expression of oxytocin, vasopressin, thyrotropin-releasing hormone, corticotropin-releasing hormone, and somatostatin, are absent in the mutant PVN, aPV, and SON. Moreover, we show that SIM1 controls the development of these secretory neurons at the final stages of their differentiation. A subset of these neuronal lineages in the PVN/SON are also missing in mice bearing a mutation in the POU transcription factor BRN2. We provide evidence that, during development of the Sim1 mutant hypothalamus, the prospective PVN/SON region fails to express Brn2. Our results strongly indicate that SIM1 functions upstream to maintain Brn2 expression, which in turn directs the terminal differentiation of specific neuroendocrine lineages within the PVN/SON.

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