Urologists
35 years of experience
Video profile
3729 Easton Nazareth Hwy
Ste LL2
Easton, PA 18045
610-253-3333
Locations and availability (3)

Education ?

Medical School Score
Drexel University (1975)
  • Currently 2 of 4 apples

Awards & Distinctions ?

Associations
American Urological Association
American Board of Urology

Affiliations ?

Dr. Walden is affiliated with 11 hospitals.

Hospital Affilations

Score

Rankings

  • St. Luke's Hospital/Bethlehem
    Urology
    801 Ostrum St, Bethlehem, PA 18015
    • Currently 4 of 4 crosses
    Top 25%
  • St Luke's Quakertown Hospital
    300 S 11th St, Quakertown, PA 18951
    • Currently 2 of 4 crosses
  • St. Luke's Miners Memorial Hospital
    360 W Ruddle St, Coaldale, PA 18218
    • Currently 2 of 4 crosses
  • Warren Hospital
    185 Roseberry St, Phillipsburg, NJ 08865
    • Currently 1 of 4 crosses
  • Easton Hospital
    Urology
    1800 East Ct, Easton, PA 18045
    • Currently 1 of 4 crosses
  • Saint Luke's Hospital - Allentown Campus
    1736 W Hamilton St, Allentown, PA 18104
  • St. Luke`s Hospital
  • Easton Hosp, Easton, Pa
  • St Lukes Health Network
  • Warren Hospital, Phillipsburg
  • Northampton dba Easton
  • Publications & Research

    Dr. Walden has contributed to 9 publications.
    Title Chronic Peroxisome Proliferator-activated Receptor Gamma (ppargamma) Activation of Epididymally Derived White Adipocyte Cultures Reveals a Population of Thermogenically Competent, Ucp1-containing Adipocytes Molecularly Distinct from Classic Brown Adipocytes.
    Date April 2010
    Journal The Journal of Biological Chemistry
    Excerpt

    The recent insight that brown adipocytes and muscle cells share a common origin and in this respect are distinct from white adipocytes has spurred questions concerning the origin and molecular characteristics of the UCP1-expressing cells observed in classic white adipose tissue depots under certain physiological or pharmacological conditions. Examining precursors from the purest white adipose tissue depot (epididymal), we report here that chronic treatment with the peroxisome proliferator-activated receptor gamma agonist rosiglitazone promotes not only the expression of PGC-1alpha and mitochondriogenesis in these cells but also a norepinephrine-augmentable UCP1 gene expression in a significant subset of the cells, providing these cells with a genuine thermogenic capacity. However, although functional thermogenic genes are expressed, the cells are devoid of transcripts for the novel transcription factors now associated with classic brown adipocytes (Zic1, Lhx8, Meox2, and characteristically PRDM16) or for myocyte-associated genes (myogenin and myomirs (muscle-specific microRNAs)) and retain white fat characteristics such as Hoxc9 expression. Co-culture experiments verify that the UCP1-expressing cells are not proliferating classic brown adipocytes (adipomyocytes), and these cells therefore constitute a subset of adipocytes ("brite" adipocytes) with a developmental origin and molecular characteristics distinguishing them as a separate class of cells.

    Title Distinct Expression of Muscle-specific Micrornas (myomirs) in Brown Adipocytes.
    Date December 2008
    Journal Journal of Cellular Physiology
    Excerpt

    MicroRNAs, a novel class of post-transcriptional gene regulators, have been demonstrated to be involved in several cellular processes regulating the expression of protein-coding genes. Here we examine murine white and brown primary cell cultures for differential expression of miRNAs. The adipogenesis-related miRNA miR-143 was highly expressed in mature white adipocytes but was low in mature brown adipocytes. Three classical "myogenic" miRNAs miR-1, miR-133a and miR-206 were absent from white adipocytes but were specifically expressed both in brown pre- and mature adipocytes, reinforcing the concept that brown adipocytes and myocytes derive from a common cell lineage that specifies energy-dissipating cells. Augmentation of adipocyte differentiation status with norepinephrine or rosiglitazone did not affect the expression of the above miRNAs, the expression levels of which were thus innately regulated. However, expression of the miRNA miR-455 was enhanced during brown adipocyte differentiation, similarly to the expression pattern of the brown adipocyte differentiation marker UCP1. In conclusion, miRNAs are differentially expressed in white and brown adipocytes and may be important in defining the common precursor cell for myocytes and brown adipocytes and thus have distinct roles in energy-storing versus energy-dissipating cells.

    Title Altered Regulation of the Pink1 Locus: a Link Between Type 2 Diabetes and Neurodegeneration?
    Date December 2007
    Journal The Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology
    Excerpt

    Mutations in PINK1 cause the mitochondrial-related neurodegenerative disease Parkinson's. Here we investigate whether obesity, type 2 diabetes, or inactivity alters transcription from the PINK1 locus. We utilized a cDNA-array and quantitative real-time PCR for gene expression analysis of muscle from healthy volunteers following physical inactivity, and muscle and adipose tissue from nonobese or obese subjects with normal glucose tolerance or type 2 diabetes. Functional studies of PINK1 were performed utilizing RNA interference in cell culture models. Following inactivity, the PINK1 locus had an opposing regulation pattern (PINK1 was down-regulated while natural antisense PINK1 was up-regulated). In type 2 diabetes skeletal muscle, all transcripts from the PINK1 locus were suppressed and gene expression correlated with diabetes status. RNA interference of PINK1 in human neuronal cell lines impaired basal glucose uptake. In adipose tissue, mitochondrial gene expression correlated with PINK1 expression although remained unaltered following siRNA knockdown of Pink1 in primary cultures of brown preadipocytes. In conclusion, regulation of the PINK1 locus, previously linked to neurodegenerative disease, is altered in obesity, type 2 diabetes and inactivity, while the combination of RNAi experiments and clinical data suggests a role for PINK1 in cell energetics rather than in mitochondrial biogenesis.

    Title Myogenic Gene Expression Signature Establishes That Brown and White Adipocytes Originate from Distinct Cell Lineages.
    Date May 2007
    Journal Proceedings of the National Academy of Sciences of the United States of America
    Excerpt

    Attainment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and increased energy expenditure potential, is a legitimate strategy for combating obesity. The unique transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our ability to promote brown adipogenesis over white. In the present work, we used microarray analysis strategies to study primary preadipocytes, and we made the striking discovery that brown preadipocytes demonstrate a myogenic transcriptional signature, whereas both brown and white primary preadipocytes demonstrate signatures distinct from those found in immortalized adipogenic models. We found a plausible SIRT1-related transcriptional signature during brown adipocyte differentiation that may contribute to silencing the myogenic signature. In contrast to brown preadipocytes or skeletal muscle cells, white preadipocytes express Tcf21, a transcription factor that has been shown to suppress myogenesis and nuclear receptor activity. In addition, we identified a number of developmental genes that are differentially expressed between brown and white preadipocytes and that have recently been implicated in human obesity. The interlinkage between the myocyte and the brown preadipocyte confirms the distinct origin for brown versus white adipose tissue and also represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid catabolism rather than storage, much like oxidative skeletal muscle tissue.

    Title Osbon Erec Aid.
    Date September 1986
    Journal The Journal of Urology
    Title Negative Cystography with Bladder Rupture: Presentation of 2 Cases and Review of the Literature.
    Date May 1980
    Journal The Journal of Urology
    Excerpt

    Cystography is commonly thought to be the sine qua non in the diagnosis of perforation or rupture of the bladder. Recently, we encountered 2 cases of bladder rupture discovered at subsequent exploration in which preoperative cystography had been negative. The reasons for these negative radiographic findings in light of a non-intact bladder are discussed and a technique for cystography is suggested that will reveal disruptions of the bladder with greater certainty.

    Title Urachal Diverticulum in a 3-year-old Boy.
    Date November 1979
    Journal The Journal of Urology
    Excerpt

    A case of a urachal diverticulum that presented as a right lower quadrant mass in a 3-year-old boy is reported. There was no urinary tract infection or obstructive uropathy in this patient. Classification of urachal anomalies is reviewed.

    Title Urethral Catheterization in Anasarca.
    Date July 1979
    Journal Urology
    Title Ovulatory Dysuria: a Bizarre Presentation of Crossed Non-fused Ectopic Kidney with Extra Renal Pelvis.
    Date
    Journal International Urology and Nephrology
    Excerpt

    Ectopic kidneys are a unique form of congenital anomaly that in most cases remain asymptomatic. However, depending on the location and the associated anatomical variations, they can mimic certain more common conditions, posing a challenge in differential diagnosis. They could cause secondary symptoms by virtue of their location or could falsely mimic a primary urologic problem when the etiology might be from a closely opposed adjacent structure. We present a unique case of ovulatory dysuria in a young female with a crossed non-fused ectopic kidney. The patient's symptoms were recurrent and correlated with the ovulatory phase of the menstrual cycle. Work-up revealed the right ovary to be in close proximity to the pelvis of the ectopic kidney. Salpingo-oophrectomy was followed by complete resolution of the patient's symptoms. The clinical manifestations, work-up, and management of symptomatic ectopic kidneys are briefly discussed in our article. Symptoms are usually attributed only by systematically excluding other causes. Surgical intervention is a last resort option only after thorough work-up with appropriate imaging studies.


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