Surgical Specialist
9 years of experience

Accepting new patients
Bergen Surgical Specialists
20 Prospect Ave
Ste 707
Hackensack, NJ 07601
201-343-0040
Locations and availability (3)

Education ?

Medical School Score Rankings
University of Pennsylvania (2001)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Awards  
2004 Fellow, Pennsylvania Safety and Leadership Academy; The Wharton School
1998 Raiffe-Gund Fellowship in Orthopedics
2007 Jonathan E Rhoads Surgical Research Award
1998 Summer Research Fellowship, National Institutes of Health
Associations
American Board of Surgery

Affiliations ?

Dr. Wilderman is affiliated with 8 hospitals.

Hospital Affilations

Score

Rankings

  • Englewood Hospital & Med Ctr
    350 Engle St, Englewood, NJ 07631
    • Currently 4 of 4 crosses
    Top 25%
  • Hackensack University Medical Center
    30 Prospect Ave, Hackensack, NJ 07601
    • Currently 4 of 4 crosses
    Top 25%
  • Morristown Memorial Hospital
    100 Madison Ave, Morristown, NJ 07960
    • Currently 3 of 4 crosses
    Top 50%
  • Pascack Valley Hospital
    250 Old Hook Rd, Westwood, NJ 07675
    • Currently 3 of 4 crosses
    Top 50%
  • St. Joseph'S Regional Medical Center
    703 Main St, Paterson, NJ 07503
    • Currently 2 of 4 crosses
  • St. Clare's Hospital-Sussex
    20 Walnut St, Sussex, NJ 07461
    • Currently 1 of 4 crosses
  • AHS Morristown Mem Hosp
  • Saint Clares Health System Denville
  • Publications & Research

    Dr. Wilderman has contributed to 7 publications.
    Title Blockade of Tnf-alpha Decreases Both Inflammation and Efficacy of Intrapulmonary Ad.ifnbeta Immunotherapy in an Orthotopic Model of Bronchogenic Lung Cancer.
    Date June 2006
    Journal Molecular Therapy : the Journal of the American Society of Gene Therapy
    Excerpt

    Adenoviral immuno-gene therapy using interferon-beta has been effective in an orthotopic model of lung cancer. However, pulmonary inflammation induced by adenoviral (Ad) vectors will almost certainly limit the maximally tolerated dose. On the other hand, the strong innate immune response generated by the vector may be helpful in initiating the adaptive immune response required for efficacy. The goals of this study were to develop an effective approach to inhibit Ad.IFNbeta-mediated acute pulmonary inflammation and to determine whether this reduction of Ad-mediated inflammation decreased the therapeutic efficacy of Ad.IFNbeta in a mouse model of bronchioloalveolar cancer. Our data show that anti-TNF-alpha antibodies can blunt the innate pulmonary immune response induced by Ad vectors, even in sensitized animals. However, this effect also inhibited the ability of the animal to generate anti-tumor immune responses and reduced survival in an orthotopic lung cancer model responsive to Ad.IFNbeta treatment. Interestingly, in a flank model of tumor using a cell line derived from the lung tumor, TNF-alpha blockade did not inhibit efficacy. These data suggest that the innate immune response to adenovirus in the lung may be important in immuno-gene therapy of lung cancer. Therapeutic application of anti-inflammatory therapy in immuno-gene therapy strategies should thus be undertaken with caution.

    Title Intrapulmonary Ifn-beta Gene Therapy Using an Adenoviral Vector is Highly Effective in a Murine Orthotopic Model of Bronchogenic Adenocarcinoma of the Lung.
    Date November 2005
    Journal Cancer Research
    Excerpt

    Given previous work showing that an adenoviral vector expressing IFN-beta (Ad.IFNbeta) was highly effective in eradicating i.p. mesothelioma tumors, the antitumor efficacy of this agent was evaluated in an orthotopic model of bronchogenic adenocarcinoma of the lung. These transgenic mice have a conditionally expressed, oncogenic K-rasG12D allele that can be activated by intratracheal administration of an adenovirus expressing Cre recombinase (Ad.Cre). K-rasG12D mutant mice were given Ad.Cre intranasally to activate the oncogene. Mice were then given 10(9) plaque-forming units of a control vector (Ad.LacZ) or Ad.IFNbeta intranasally 3 and 4 weeks later, a time when lung tumors had been established. Cells derived from K-ras-mutated lung tumors were also grown in the flanks of mice to study mechanisms of therapeutic responses. In two separate experiments, untreated tumor-bearing mice all died by day 57 (median survival, 49 days). Ad.LacZ-treated mice all died by day 71 (median survival, 65 days). In contrast, 90% to 100% of mice treated with Ad.IFNbeta were long-term survivors (>120 days; P < 0.001). In addition, immunity to re-challenge with tumor cells was induced. In vitro and flank tumor studies showed that Ad.IFNbeta induced direct tumor cell killing and that depleting natural killer or CD8+ T cells, but not CD4+ T cells, with antibodies attenuated the effect of Ad.IFNbeta. These studies, showing remarkable antitumor activity in this orthotopic lung cancer model, provide strong preclinical support for a trial of Ad.IFNbeta to treat human non-small cell lung cancer.

    Title Role of Endothelial Nitric Oxide Synthase in Hypoxia-induced Pial Artery Dilation.
    Date June 1998
    Journal Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
    Excerpt

    Nitric oxide (NO) contributes to hypoxia-induced pial artery dilation, at least in part, through the formation of cGMP and the subsequent release of methionine enkephalin and leucine enkephalin in the newborn pig. In separate studies, these opioids also were observed to elicit NO-dependent pial artery dilation, whereas light/dye endothelial injury reduced hypoxic pial dilation. The current study was designed to investigate the role of the endothelial isoform of NO synthase in hypoxic pial dilation, associated opioid release, and opioid dilation in piglets equipped with a closed cranial window. N-iminoethyl-L-ornithine (L-NIO) (10(-6) mol/L), an antagonist that may have greater endothelial NO synthase inhibitory selectivity, had no effect on dilation elicited by hypoxia (PO2 approximately 35 mm Hg) (24 +/- 2 versus 24 +/- 2% in the absence and presence of L-NIO, respectively, n = 8). Hypoxic dilation was accompanied by increased CSF cGMP, which also was unchanged in the presence of L-NIO (394 +/- 19 and 776 +/- 63 versus 323 +/- 13 and 739 +/- 25 fmol/mL for control and hypoxia in the absence and presence of L-NIO, respectively, n = 6). Additionally, hypoxic pial dilation was associated with increased CSF methionine enkephalin, which also was unchanged in the presence of L-NIO (992 +/- 73 and 2469 +/- 197 versus 984 +/- 18 and 2275 +/- 185 pg/mL, respectively, n = 6). In contrast, methionine enkephalin-induced dilation was blocked by L-NIO (6 +/- 1, 10 +/- 1, and 16 +/- 1 versus 1 +/- 1, 1 +/- 1, and 2 +/- 1% for 10(-10), 10(-8), 10(-6) mol/L methionine enkephalin, respectively, before and after L-NIO, n = 8). Substance P-induced pial dilation was blunted by L-NIO, whereas responses to sodium nitroprusside and N-methyl-D-aspartate were unchanged. These data indicate that endothelial NO synthase contributes to opioid-induced pial artery dilation but not hypoxia-induced dilation. Additionally, these data suggest that neuronally derived NO contributes to hypoxic pial dilation.

    Title Role of Neuronal No Synthase in Relationship Between No and Opioids in Hypoxia-induced Pial Artery Dilation.
    Date December 1997
    Journal The American Journal of Physiology
    Excerpt

    Nitric oxide (NO) contributes to hypoxia-induced pial artery dilation, at least in part, via the formation of guanosine 3',5'-cyclic monophosphate (cGMP) and subsequent release of Met-enkephalin and Leu-enkephalin in the newborn pig. In separate studies, these opioids were also observed to elicit NO-dependent pial dilation. The present study was designed to investigate the role of the neuronal isoform of NO synthase (NOS) in hypoxic pial dilation, associated opioid release, and opioid dilation in piglets equipped with a closed cranial window. Tetrodotoxin (10(-6) M) attenuated the dilation resulting from hypoxia (PO2 approximately 35 mmHg; 25 +/- 1 vs. 14 +/- 1%). Similarly, 7-nitroindazole, sodium salt (7-NINA, 10(-6) M), a purported neuronal NOS inhibitor, attenuated hypoxic pial dilation (26 +/- 1 vs. 14 +/- 2%). Hypoxic dilation was accompanied by elevated cerebrospinal (CSF) cGMP, which was blocked by 7-NINA (433 +/- 19 and 983 +/- 36 vs. 432 +/- 19 and 441 +/- 19 fmol/ml for control and hypoxia in absence and presence of 7-NINA, respectively). Additionally, hypoxic dilation was also accompanied by elevated CSF Met-enkephalin, which was attenuated by 7-NINA (1,027 +/- 47 and 2,871 +/- 134 vs. 779 +/- 78 and 1,551 +/- 42 pg/ml for control and hypoxia in absence and presence of 7-NINA, respectively). In contrast, Met-enkephalin (10(-10), 10(-8), and 10(-6) M) induced dilation that was unchanged by 7-NINA (7 +/- 1, 12 +/- 1, and 18 +/- 1 vs. 6 +/- 1, 10 +/- 1, and 17 +/- 1%, respectively). N-methyl-D-aspartate (NMDA, 10(-8) and 10(-6) M), an activator of neuronal NOS, induced pial dilation that was blocked by 7-NINA (10 +/- 1 and 20 +/- 2 vs. 1 +/- 1 and 2 +/- 1%, respectively). However, sodium nitroprusside-induced dilation was unchanged by 7-NINA. These data indicate that neuronal NOS contributes to hypoxic pial artery dilation but not to opioid-induced dilation. Furthermore, these data suggest that neuronally derived NO contributes to hypoxic dilation, at least in part, via formation of cGMP and the subsequent release of opioids.

    Title Role of Pacap in the Relationship Between Camp and Opioids in Hypoxia-induced Pial Artery Vasodilation.
    Date April 1997
    Journal The American Journal of Physiology
    Excerpt

    The opioids methionine enkephalin and leucine enkephalin contribute to hypoxic pial artery dilation in the newborn pig, and adenosine 3',5'-cyclic monophosphate (cAMP) analogs have been shown to elevate cerebrospinal fluid (CSF) opioid concentration. The present study was designed to investigate the contribution of cAMP to hypoxic dilation and to determine whether an endogenous activator of adenylate cyclase, pituitary adenylate cyclase-activating peptide (PACAP), could modulate the cAMP-induced release of opioids to contribute to hypoxic pial dilation in piglets equipped with closed cranial windows. An alpha level of P < 0.05 was considered significant in all statistical tests. Moderate and severe hypoxia (PO2 approximately 35 and 25 mmHg, respectively) induced pial artery dilation that was attenuated by the Rp diastereomer of 8-bromoadenosine 3',5'-cyclic monophosphothioate (Rp-8-BrcAMPS), a cAMP antagonist (24 +/- 1 and 36 +/- 2% vs. 21 +/- 1 and 30 +/- 1% for moderate hypoxia and 34 +/- 1 and 46 +/- 2% vs. 24 +/- 1 and 32 +/- 1% for severe hypoxia before and after Rp-8-BrcAMPS, respectively). These responses were associated with an increased CSF cAMP (1,046 +/- 25, 1,366 +/- 28, and 1,735 +/- 47 fmol/ml for control, moderate, and severe hypoxia, respectively). Hypoxic pial dilation was also accompanied by an increase in CSF methionine enkephalin (1,101 +/- 62, 3,283 +/- 119, and 3,835 +/- 129 pg/ml for control, moderate, and severe hypoxia, respectively). Hypoxic dilation additionally increased CSF PACAP (1,727 +/- 86, 2,268 +/- 157, and 7,980 +/- 238 pg/ml for control, moderate, and severe hypoxia, respectively). PACAP (10(-8) and 10(-6) M) elicited pial dilation that was associated with increased CSF cAMP and blunted by Rp-8-BrcAMPS. PACAP-induced dilation was also accompanied by increases in the opioid methionine enkephalin (1,059 +/- 23, 1,483 +/- 34, and 2,108 +/- 77 pg/ml for control and 10(-8) and 10(-6) M PACAP, respectively). These data show that cAMP contributes to hypoxic pial artery dilation. Hypoxia increases CSF PACAP, whereas PACAP elevates CSF opioid concentration. These data, therefore, suggest that PACAP modulates cAMP-induced opioid release, thereby contributing to hypoxic pial dilation.

    Title Influence of Camp on Cerebrospinal Fluid Opioid Concentration: Role in Camp-induced Pial Artery Dilation.
    Date January 1997
    Journal European Journal of Pharmacology
    Excerpt

    Previously, it has been observed that cGMP analogs and agents that elevate cGMP levels markedly increase the concentration of the opioids [Met5]enkephalin and [Leu5]enkephalin in cortical periarachnoid cerebrospinal fluid (CSF) of the newborn pig. However, such agents had no effect on CSF dynorphin-(1-13) concentration. The present study was designed to: (1) investigate the influence of cAMP on the CSF concentration of the opioids [Met5]enkephalin, [Leu5]enkephalin and dynorphin-(1-13); and (2) determine the role of these opioids in cAMP-induced pial artery vasodilation. Piglets equipped with closed cranial windows were used to measure pial artery diameter and collect cortical periarachnoid CSF for assay of opioids. The cAMP analog, 8-Bromoadenosine-3',5'-cyclic monophosphate (8-Bromo cAMP) elicited pial dilation that was blunted by a cAMP antagonist, Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate (10(-5) M) (11 +/- 1 and 19 +/- 1 vs. 1 +/- 1 and 1 +/- 1 for 10(-8) M, 10(-6) M 8-Bromo cAMP before and after Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate, respectively). The dilation produced by 8-Bromo cAMP was accompanied by modest increases in CSF [Met5]enkephalin and co-administration of Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate with 8-Bromo cAMP blocked these increases in CSF opioid concentration (1179 +/- 48, 1593 +/- 92 and 2079 +/- 88 vs. 1054 +/- 32, 1038 +/- 15 and 1071 +/- 17 pg/ml for control, 10(-8) M and 10(-6) M 8-Bromo cAMP before and after Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate, respectively). The release of CSF [Leu5]enkephalin by 8-Bromo cAMP was also blocked by Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate. In contrast 8-Bromo cAMP produced marked increases in CSF dynorphin-(1-13) (38 +/- 3, 61 +/- 3 and 88 +/- 6 vs. 27 +/- 3, 28 +/- 3 and 30 +/- 4 pg/ml for control, 10(-8) M and 10(-6) M 8-Bromo cAMP before and after Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate, respectively). Similar blunted vascular and biochemical responses were observed with the co-administration of Sp 8-Bromoadenosine-3',5'-cyclic monophosphorothioate, another analog of cAMP, with Rp 8-Bromoadenosine-3',5'-cyclic monosphorothioate. The opioid receptor antagonist naloxone (1 mg/kg i.v.) attenuated 8-Bromo cAMP-induced dilation (9 +/- 1 and 17 +/- 1 vs. 5 +/- 1 and 8 +/- 1 for 10(-8) M, 10(-6) M 8-Bromo cAMP before and after naloxone). These data show that cAMP contributes to the release of the CSF opioids [Met5]enkephalin, [Leu5]enkephalin and dynorphin-(1-13), and suggest that, while cGMP is more important relative to cAMP in elevating CSF [Met5]enkephalin and [Leu5]enkephalin concentration, the converse is true for dynorphin-(1-13). Further, these data indicate that opioids contribute to cAMP-induced pial artery vasodilation.

    Title Relationship Between Nitric Oxide and Opioids in Hypoxia-induced Pial Artery Vasodilation.
    Date October 1996
    Journal The American Journal of Physiology
    Excerpt

    It has previously been observed that nitric oxide (NO) and the opioids Met- and Leu-enkephalin contribute to hypoxia-induced pial artery dilation in the newborn pig. The present study was designed to investigate the relationship between NO and opioids in hypoxic pial dilation. Piglets equipped with closed cranial windows were used to measure pial artery diameter and collect cortical periarachnoid cerebrospinal fluid (CSF) for assay of opioids. Sodium nitroprusside (SNP; 10(-8) and 10(-6) M) elicited pial dilation that was blunted by the soluble guanylate cyclase inhibitor LY-83583 (10(-5) M; 10 +/- 1 and 23 +/- 1 vs. 3 +/- 1 and 7 +/- 1% for 10(-8) and 10(-6) M SNP before and after LY-83583, respectively). SNP-induced dilation was accompanied by increased CSF Met-enkephalin, and coadministration of LY-83583 with SNP blocked these increases in CSF opioid concentration (1,144 +/- 59, 2,215 +/- 165, and 3,413 +/- 168 vs. 1,023 +/- 16, 1,040 +/- 18, and 1,059 +/- 29 pg/ml for control and 10(-8) and 10(-6) M SNP before and after LY-83583, respectively). SNP-induced release of CSF Leuenkephalin was also blocked by LY-83583. Similar blunted vascular and biochemical effects of SNP were observed with coadministration of the purported guanosine 3', 5'-cyclic monophosphate (cGMP) antagonist, the phosphorothioate analogue of 8-bromo-cGMP (BrcGMP) [(R)-p-BrcGMP[S]; 10(-5) M]. The cGMP analogue, BrcGMP, elicited dilation that was also accompanied by increased CSF Met- and Leu-enkephalin. Vascular and biochemical effects of BrcGMP were blunted by (R)-p-cGMP[S] and unchanged by LY-83583. Hypoxia-induced pial artery dilation was attenuated by N omega-nitro-L-arginine (L-NNA; 10(-6) M), an NO synthase inhibitor (25 +/- 2 vs. 14 +/- 1%). Hypoxic pial dilation was accompanied by increased CSF Met-enkephalin, and these increases were attenuated by L-NNA (1,137 +/- 60 and 3,491 +/- 133 vs. 927 +/- 25 and 2,052 +/- 160 pg/ml for control and hypoxia before and after L-NNA, respectively). Hypoxia also increased CSF Leuenkephalin, and these CSF changes were similarly attenuated by L-NNA. These data show that cGMP increases CSF Met- and Leu-enkephalin. Furthermore, these data suggest that NO contributes to hypoxic dilation, at least in part, via formation of cGMP and the subsequent release of opioids.


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