Gene F Coppa

Hofstra North Shore-LIJ School of Medicine, New York, New York, United States

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Publications (70)200.65 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Total colectomy with ileostomy placement is a treatment for patients with inflammatory bowel disease or familial adenomatous polyposis (FAP). A rare and late complication of this treatment is carcinoma arising at the ileostomy site. We describe two such cases: a 78-year-old male 30 years after subtotal colectomy and ileostomy for FAP, and an 85-year-old male 50 years after colectomy and ileostomy for ulcerative colitis. The long latency period between creation of the ileostomies and development of carcinoma suggests a chronic metaplasia due to an irritating/inflammatory causative factor. Surgical excision of the mass and relocation of the stoma is the mainstay of therapy, with possible benefits from adjuvant chemotherapy. Newly developed lesions at stoma sites should be biopsied to rule out the possibility of this rare ileostomy complication.
    06/2015; 7(6):94-7. DOI:10.4240/wjgs.v7.i6.94
  • International Journal of Angiology 05/2015; DOI:10.1055/s-0034-1376317
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    ABSTRACT: Cutaneous wound continues to cause significant morbidity and mortality in the setting of diseases such as diabetes and cardiovascular diseases. Despite advances in wound care management, there is still an unmet medical need exists for efficient therapy for cutaneous wound. Combined treatment of adrenomedullin (AM) and its binding protein-1 (AMBP-1) is protective in various disease conditions. To examine the effect of the combination treatment of AM and AMBP-1 on cutaneous wound healing, full-thickness 2.0-cm diameter circular excision wounds were surgically created on the dorsum of rats, saline (vehicle) or AM/AMBP-1 (96/320 μg kg BW) was topically applied to the wound daily and wound size measured. At days 3, 7, and 14, skin samples were collected from the wound sites. AM/AMBP-1 treated group had significantly smaller wound surface area than the vehicle group over the 14-day time course. At day 3, AM/AMBP-1 promoted neutrophil infiltration (MPO), increased cytokine levels (IL-6 and TNF-α), angiogenesis (CD31, VEGF and TGFβ-1) and cell proliferation (Ki67). By day 7 and 14, AM/AMBP-1 treatment decreased MPO, followed by a rapid resolution of inflammation characterized by a decrease in cytokines. At the matured stage, AM/AMBP-1 treatment increased the alpha smooth muscle actin expression (mature blood vessels) and Masson-Trichrome staining (collagen deposition) along the granulation area, and increased MMP-9 and decreased MMP-2 mRNA expressions. TGFβ-1 mRNA levels in AM/AMBP-1 group were 5.3 times lower than those in the vehicle group. AM/AMBP-1 accelerated wound healing by promoting angiogenesis, collagen deposition and remodeling. Treatment also shortened the days to reach plateau for wound closure. Thus, AM/AMBP-1 may be further developed as a therapeutic for cutaneous wound healing.
    PLoS ONE 03/2015; 10(3):e0120225. DOI:10.1371/journal.pone.0120225 · 3.53 Impact Factor
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    ABSTRACT: Hemorrhagic shock is a leading cause of morbidity and mortality in surgery and trauma patients. Despite a large number of preclinical trials conducted to develop therapeutic strategies against hemorrhagic shock, there is still an unmet need for effective therapy for hemorrhage patients. Wnt/β-catenin signaling controls developmental processes and cellular regeneration owing to its central role in cell survival and proliferation. We therefore hypothesized that the activation of Wnt signaling reduces systemic injury caused by hemorrhagic shock. Adult male Sprague-Dawley rats underwent hemorrhagic shock by controlled bleeding of the femoral artery to maintain a mean arterial pressure of 30 mm Hg for 90 minutes, followed by resuscitation with crystalloid equal to two times the shed blood volume. After resuscitation, animals were infused with Wnt agonist (5 mg/kg) or vehicle (20% dimethyl sulfoxide in saline). Blood and tissue samples were collected 6 hours after resuscitation for analysis. Hemorrhagic shock increased serum levels of aspartate aminotransferase, lactate, and lactate dehydrogenase. Treatment with Wnt agonist significantly reduced these levels by 40%, 36%, and 77%, respectively. Wnt agonist also decreased blood urea nitrogen and creatinine by 34% and 56%, respectively. The treatment reduced lung myeloperoxidase activity and interleukin 6 messenger RNA by 55% and 68%, respectively, and significantly improved lung histology. Wnt agonist treatment increased Bcl-2 protein to sham values and decreased cleaved caspase 3 by 46%, indicating attenuation of hemorrhage-induced apoptosis in the lungs. Hemorrhage resulted in significant reductions of β-catenin protein levels in the lungs as well as down-regulation of a Wnt target gene, cyclin D1, while Wnt agonist treatment preserved these levels. The administration of Wnt agonist attenuated hemorrhage-induced organ injury, inflammation, and apoptosis. This was correlated with the preservation of the Wnt signaling pathway. Thus, Wnt/β-catenin activation could be protective in hemorrhagic shock.
    Journal of Trauma and Acute Care Surgery 03/2015; 78(4). DOI:10.1097/TA.0000000000000566 · 1.97 Impact Factor
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    ABSTRACT: Intestinal ischemia-reperfusion (I/R) is encountered in various clinical conditions and contributes to multi organ failure and mortality as high as 60-80%. Intestinal I/R not only injures the intestine but affects remote organs such as the lung leading to acute lung injury. The development of novel and effective therapies for intestinal I/R are critical for the improvement of patient outcome. AICAR is a cell permeable compound that has shown to possess anti-inflammatory effects. The objective is to determine that treatment with AICAR attenuates intestinal I/R injury and subsequent acute lung injury (ALI). Male Sprague-Dawley rats (275-325 g) underwent intestinal I/R injury with blockage of the superior mesenteric artery for 90 min and subsequently reperfusion. At the initiation of reperfusion, vehicle or AICAR (30 mg/kg BW) were given IV for 30 min. At 4 h after reperfusion, blood and tissues were collected for further analyses. Treatment with AICAR significantly decreased the gut damage score and the water content indicating improvement in histological integrity. The treatment also attenuated tissue injury and proinflammatory cytokines, and reduced bacterial translocation to the gut. AICAR administration after intestinal I/R maintained lung integrity, attenuated neutrophil chemotaxis and infiltration to the lungs, and decreased lung levels of TNF-α and IL-6. Inflammatory mediators, iNOS and COX-2 proteins, were decreased in the lungs and lung apoptosis were significantly reduced after AICAR treatment. These data indicate that AICAR could be developed as an effective and novel therapeutic for intestinal I/R and subsequent ALI.
    Molecular Medicine 01/2015; 20. DOI:10.2119/molmed.2014.00134 · 4.82 Impact Factor
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    International Journal of Angiology 01/2015; DOI:10.1055/s-0034-1396947
  • 15th Annual State of the Art Winter Symposium of the; 01/2015
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    ABSTRACT: Renal ischemia-reperfusion (IR) injury (IRI) following shock states or transplantation causes tissue damage and delayed graft function, respectively. The Wnt/β-catenin signaling pathway plays a critical role in nephrogenesis. We therefore hypothesized that pharmacological activation of Wnt/β-catenin signaling by Wnt agonist, a synthetic pyrimidine, could protect kidneys from IRI. Adult male rats were subjected to bilateral clamping of the renal pedicles with microvascular clips for 60 min, followed by reperfusion. Wnt agonist (5 mg/kg BW) or vehicle (20% DMSO in saline) was administered intravenously 1 h prior to ischemia. Blood and renal tissues were collected 24 h after IR for evaluation. Renal IR caused a significant reduction of β-catenin and its downstream target gene cyclin D1 by 65% and 39%, respectively, compared to the sham, while Wnt agonist restored them to the sham levels. The number and intensity of cells staining with the proliferation marker Ki67 in ischematized kidneys were enhanced by Wnt agonist. The integrity of the renal histological architecture in the Wnt agonist group was better preserved than the vehicle group. Wnt agonist significantly lowered serum levels of creatinine, AST, and LDH, inhibited the production of IL-6 and IL-1β, and MPO activities. Lastly, Wnt agonist reduced iNOS, nitrotyrosine proteins and 4-hydroxynonenal in the kidneys by 60%, 47% and 21%, respectively, compared to the vehicle. These results indicate that Wnt agonist improves renal regeneration and function while attenuating inflammation and oxidative stress in the kidneys after IR. Thus, pharmacologic stimulation of Wnt/β-catenin signaling provides a beneficial effect on the prevention of renal IRI.
    Shock (Augusta, Ga.) 11/2014; 179(2). DOI:10.1097/SHK.0000000000000293 · 2.73 Impact Factor
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    ABSTRACT: With the ability to identify the presence of transforming colonocytes in a field adjacent to an existing primary colon cancer, it is now possible to reduce if not eliminate one of the major causes leading to anastomotic tumor recurrence. In a review of those colectomy cases that presented post-surgery with anastomotic recurrence, we noted that mucosal abnormalities could readily be detected adjacent to the primary lesion. Such changes had gone unrecognized at the time of surgery, when standard histologic procedures were employed. By utilizing monoclonal antibodies (mAbs) that defined the presence of tumor immunogenic proteins, we were able to reexamine so-called normal biopsy sites adjacent to the tumor. Here, it was possible to demonstrate the presence of altered cellular activity in existing phenotypically normal appearing colonocytes that were in the process of transforming to malignancy. Eight consecutive patients that had been admitted for evaluation and resection of an anastomotic recurrence post colectomy, were studied with regard to possible etiologic factors. The original margins incorporated into the anastomosis were re-examined by immunohistochemistry employing those monoclonal antibodies (mAbs) designed to target colon tumor antigen. This antigen had previously been shown to be expressed only in colon cancer and not in adjacent normal tissue. In addition, biopsies from margins of resection in five patients free of recurrence following colectomy were also studied along with colon specimens from 50 normal patients, non-demonstrating expression of tumor antigen in the normal appearing colonocytes. In each of the patients who had presented with anastomotic recurrence, normal appearing colonocytes defined by light microscopy and found adjacent to the previously resected primary lesion, expressed tumor antigen. The antigen detected in these colonocytes proved to be identical to antigen expressed in the anastomotic recurrence giving credence to the concept that these normal appearing cells in proximity to the tumor were responsible for the regrowth of tumor in the suture line used to establish continuity of the bowel. Based on the findings of this preliminary retrospective study it is felt that at the time of performing a colectomy for a malignant lesion of the bowel, that it is important that those normal appearing colonocytes adjacent to tumor be evaluated for expression of tumor associated antigen. Excluding such cells from an anastomosis, may help to assure that tumor recurrence will be minimized if not totally eliminated.
    Journal of Cancer 10/2014; 5(9):784-9. DOI:10.7150/jca.9485 · 2.64 Impact Factor
  • Journal of the American College of Surgeons 09/2014; 219(3):S39. DOI:10.1016/j.jamcollsurg.2014.07.085 · 4.45 Impact Factor
  • Journal of the American College of Surgeons 09/2014; 219(3):S38-S39. DOI:10.1016/j.jamcollsurg.2014.07.084 · 4.45 Impact Factor
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    ABSTRACT: Cold inducible RNA-binding protein (CIRP) is a nuclear protein which has been recently identified as a novel inflammatory mediator in hemorrhagic shock and sepsis. We hypothesized that CIRP acts as a potent inflammatory mediator in hepatic ischemia-reperfusion (I/R), and thus blocking CIRP protects against I/R-induced liver injury. Male C57BL/6 mice were subjected to 70% hepatic ischemia by microvascular clamping of the hilum of the left and median liver lobes for 60 min, followed by reperfusion. Anti-CIRP antibody (1 mg/kg body weight) or vehicle (normal saline) in 0.2 mL was injected via the internal jugular vein at the beginning of the reperfusion. Blood and liver tissues were collected 24 h after I/R for various measurements and a 10-day survival study was performed. CIRP released into the circulation was significantly increased 24 h after hepatic I/R. Anti-CIRP antibody treatment markedly reduced hepatocellular damage markers and significantly improved the liver microarchitecture. Anti-CIRP also reduced the systemic and local inflammation demonstrated by attenuation in both serum and hepatic levels of interleukin 6. The expression of neutrophil-attracting chemokine as well as liver neutrophil infiltration was reduced by anti-CIRP treatment. Anti-CIRP also dramatically decreased the amount of apoptosis and nitrosative stress, evidenced by decrease in TUNEL staining and inducible nitric oxide synthase and cyclooxygenase-2 levels, respectively. Finally, the 10-day survival rate was increased from 37.5% in the vehicle group to 75% in the anti-CIRP treatment group. Thus, targeting CIRP offers potential therapeutic implications in the treatment of hepatic I/R injury.
    Shock (Augusta, Ga.) 08/2014; 43(1). DOI:10.1097/SHK.0000000000000251 · 2.73 Impact Factor
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    ABSTRACT: Background Renal ischemia-reperfusion (I/R) is a severe clinical complication with no specific treatment. Resveratrol has been shown as a promising experimental agent in renal I/R due to its effect on cellular energy metabolism, oxidative stress, and inflammation. Recently, we identified two biologically active resveratrol analogues (RSVAs), RSVA405 and RSVA314. We hypothesized that both RSAVs would attenuate I/R-induced renal injury. Methods Adult male rats were subjected to renal I/R through bilateral renal pedicle clamping for 60 min, followed by reperfusion. RSVA405 (3 mg/kg BW), RSVA314 (3 mg/kg BW), or vehicle (10% DMSO and 33% Solutol in PBS) was administered by intraperitoneal injection 1 h prior to ischemia. Blood and renal tissues were collected 24 h after I/R for evaluation. Results Administration of RSVA405 and RSVA314 significantly reduced the serum levels of renal dysfunction and injury markers, including creatinine, blood urea nitrogen, aspartate aminotransferase, and lactate dehydrogenase, compared to vehicle. The protective effect of RSVA405 and RSVA314 was also reflected on histologic evaluation. Both RSVAs reduced the number of apoptotic cells by more than 60% as determined by TUNEL assay, compared to vehicle. The renal ATP levels of the vehicle group was decreased to 52.4% of control, while those of the RSVA405 and RSVA314 groups were restored to 72.3% and 79.6% of control, respectively. Both RSVAs significantly reduced the protein expression of inducible nitric oxide synthase and nitrotyrosine, and the mRNA levels of TNF-α, IL-6 and IL-1β. Conclusions RSVA405 and RSVA314 attenuate I/R-induced renal injury through the modulation of energy metabolism, oxidative stress, and inflammation.
    Journal of Surgical Research 08/2014; 193(2). DOI:10.1016/j.jss.2014.08.015 · 2.12 Impact Factor
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    ABSTRACT: In an attempt to improve upon the end results obtained in treating colorectal cancer it was apparent that the earlier the diagnosis that could be obtained, the better the chance for obtaining desired results. In the case of more advanced tumors typified by later stage colorectal cancer, surgical debulking is an important part of the treatment strategy. Here the use of additional therapeutic modalities including chemotherapy and present day immunotherapy has failed to accomplish the desired improvements that have been sought after. Adjuvant therapy, has offered little to the overall survival. The concept of early detection is now recognized as the initial step in reaching proper end results and can readily be demonstrated from colorectal cancer studies. Here survival has been found to be a reflection of the stage at which the tumor is first identified and treated. When specific monoclonals targeting colorectal cancer are employed diagnostically, we have been able to demonstrate detection of colorectal cancer at its inception as a premalignant lesion, such that genotypic features can be identified before the phenotypic appearance of cancer can be noted.
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    ABSTRACT: Renal ischemia-reperfusion (I/R) is a major contributor to delayed graft function after renal transplantation. The pathophysiology of I/R can be summarized by a primary energy deficit during ischemia and a secondary phase of oxidative stress and inflammation. Sirtuin 1 is an energy-sensing enzyme involved in regulating multiple cellular functions. We hypothesized that stimulating Sirtuin 1 would increase mitochondrial biogenesis thereby enhancing energy metabolism and attenuating I/R-induced renal injury.
    Transplantation 06/2014; 217(3). DOI:10.1097/TP.0000000000000194 · 3.78 Impact Factor
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    ABSTRACT: To determine the mechanism responsible for ghrelin's neuroprotective effects after traumatic brain injury (TBI) and hemorrhagic shock. Ghrelin, a gastrointestinal hormone, has been demonstrated to possess multiple functions, including upregulation of uncoupling protein 2 (UCP2) and stimulation of the vagus nerve. Recent evidence has indicated that ghrelin is neuroprotective. We, therefore, hypothesized that ghrelin protects rats against TBI and hemorrhagic shock through upregulation of UCP2, involving stimulation of the vagus nerve. Brain injury was induced by dropping a 450 g of weight from 1.5 m onto a steel helmet attached to the skull of male adult rats. Immediately after TBI, a midline laparotomy was performed, and both lumbar veins were isolated and severed at the junction with the vena cava. The abdomen was kept open for 20 minutes. At 45 minutes after TBI and uncontrolled hemorrhage (UH), ghrelin (4, 8, or 16 nmol/rat) or 1 mL of normal saline (vehicle) was intravenously administered. The Neurological Severity Scale (NSS), morphological alterations and β-amyloid precursor protein expression in the brain, systemic organ injury markers (ie, alanine aminotransferase, aspartate aminotransferase, and lactate), and UCP2 expression in the cortex were measured. To determine whether the protective effect of ghrelin is mediated through upregulation of UCP2, genipin, a specific UCP2 antagonist, was administered intravenously before the injection of ghrelin in animals with TBI and UH. The role of the vagus nerve was assessed by performing vagotomy immediately before ghrelin administration. Ghrelin attenuated brain injury and facilitated functional recovery after TBI and UH. Ghrelin increased UCP2 expression in the cortex, and administration of genipin abolished ghrelin's protection after TBI and UH. Furthermore, vagotomy prevented the beneficial effects of ghrelin and eliminated ghrelin-induced UCP2 upregulation after TBI and UH. The protective effects of ghrelin after TBI and UH seem to be related to upregulation of UCP2 expression in the brain and requiring the intact vagus nerve.
    Annals of surgery 03/2014; 260(1). DOI:10.1097/SLA.0000000000000328 · 7.19 Impact Factor
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    ABSTRACT: Enteric drainage is the preferred method of exocrine diversion in simultaneous kidney-pancreas transplantation. Because of improvements in immunosuppression, enteric drainage has become the preferred method of pancreas transplantation in general. Although associated with less potential complications than bladder-drained pancreas, potentially lethal arterio-enteric fistulas in the setting of nonfunctioning allografts represent a constant threat. We herein present a case report, a review of the literature, and a call for caution.
    International Journal of Angiology 03/2014; 23(1):65-8. DOI:10.1055/s-0033-1349169
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    ABSTRACT: This study sought to examine various factors that may prevent transplant candidates from completing their transplant workup prior to listing. We reviewed the records of 170 subjects (cases = 100, controls 70) who were either on dialysis or had less than 20 mL/min creatinine clearance and were therefore candidates for preemptive transplantation. Approximately, 56% of preemptive patients completed their workup, while only 36% of patients on dialysis completed their workup. Our data revealed that factors contributing toward completion of workup included intrinsic motivation (four times more likely), lack of specific medical comorbidities (three times more likely), and preemptive status (two times more likely). Among patients on dialysis, intrinsic motivation (five times more likely) and absence of cardiovascular complications (four times more likely) were associated with completion. When comparing patients on dialysis to patients not on dialysis, there were significant differences between the two groups in distance from home to the transplant center, level of education, and presence of medical comorbidities. We believe that targeted interventions such as timely referral, providing appropriate educational resources, and development of adequate support systems, have the potential to improve workup compliance of patients with advanced chronic kidney disease, including those on dialysis.
    International Journal of Angiology 03/2014; 23(1):23-8. DOI:10.1055/s-0033-1358661
  • Journal of Surgical Research 02/2014; 186(2):584. DOI:10.1016/j.jss.2013.11.527 · 2.12 Impact Factor
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    ABSTRACT: Laparoscopic Roux-en-Y gastric bypass is indicated in the treatment of morbid obesity. This chapter details indications, pitfalls, technique, and complications associated with this procedure.
    Chassin's Operative Strategy in General Surgery, 01/2014: pages 373-381; , ISBN: 978-1-4614-1392-9

Publication Stats

259 Citations
200.65 Total Impact Points


  • 2011–2015
    • Hofstra North Shore-LIJ School of Medicine
      New York, New York, United States
  • 2013
    • Hofstra University
      Хемпстед, New York, United States
  • 2009–2013
    • North Shore-Long Island Jewish Health System
      • Department of Surgery
      New York City, New York, United States
  • 2012
    • North Shore-LIJ Health System
      • Department of Surgery
      Manhasset, New York, United States
  • 2009–2011
    • The Feinstein Institute for Medical Research
      • Center for Immunology and Inflammation
      New York City, NY, United States
  • 1999–2005
    • Staten Island University Hospital
      New York, United States