Gene F Coppa

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

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Publications (49)131.82 Total impact

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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 (Cambridge, Mass.). 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; · 2.87 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; · 2.87 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; · 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.
    World journal of gastrointestinal oncology. 06/2014; 6(6):170-176.
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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; · 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; · 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.
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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.
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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. 01/2014; 5(9):784-9.
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    ABSTRACT: A systemic inflammatory response is observed in patients undergoing hemorrhagic shock and sepsis. Here we report increased levels of cold-inducible RNA-binding protein (CIRP) in the blood of individuals admitted to the surgical intensive care unit with hemorrhagic shock. In animal models of hemorrhage and sepsis, CIRP is upregulated in the heart and liver and released into the circulation. In macrophages under hypoxic stress, CIRP translocates from the nucleus to the cytosol and is released. Recombinant CIRP stimulates the release of tumor necrosis factor-α (TNF-α) and HMGB1 from macrophages and induces inflammatory responses and causes tissue injury when injected in vivo. Hemorrhage-induced TNF-α and HMGB1 release and lethality were reduced in CIRP-deficient mice. Blockade of CIRP using antisera to CIRP attenuated inflammatory cytokine release and mortality after hemorrhage and sepsis. The activity of extracellular CIRP is mediated through the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 2 (MD2) complex. Surface plasmon resonance analysis indicated that CIRP binds to the TLR4-MD2 complex, as well as to TLR4 and MD2 individually. In particular, human CIRP amino acid residues 106-125 bind to MD2 with high affinity. Thus, CIRP is a damage-associated molecular pattern molecule that promotes inflammatory responses in shock and sepsis.
    Nature medicine 10/2013; · 28.05 Impact Factor
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    ABSTRACT: Sepsis is an acute inflammatory condition that can result in multiple organ failure and acute lung injury (ALI). Growth arrest-specific protein 6 (Gas6) is a broad regulator of the innate immune response involved with the NF-κB signaling pathway. We hypothesized that Gas6 could have a protective role in attenuating the severity of ALI and sepsis. Male mice were subjected to sepsis by cecal ligation and puncture (CLP) after which recombinant murine Gas6 (rmGas6; 5 μg/mouse) or normal saline (vehicle) was administered intravenously. Blood and lung tissues were collected at 20 h after CLP for various measurements. Treatment with rmGas6 significantly reduced serum levels of the injury markers AST, ALT and LDH as well as proinflammatory cytokines IL-6 and IL-17, compared to the vehicle group (P<0.05). The parenchyma of the lungs damaged by CLP was attenuated by rmGas6 treatment. Lung mRNA levels of TNF-α, IL-1β, IL-6, IL-17 and MIP-2 were decreased by 60%, 86%, 82%, 93% and 82%, respectively, with rmGas6 treatment as determined by real time RT-PCR (P<0.05). The degradation of IκB-α induced by CLP in the lungs was inhibited by rmGas6 treatment. The number of neutrophils and myeloperoxidase activity in the lungs were significantly reduced in the rmGas6 group. Moreover, rmGas6 reduced the in-vitro migration of differentiated human promyelocytic HL60 cells by 64%. Finally, the 10-day survival rate of mice subjected to CLP was increased from 31% in the vehicle group to 67% in the rmGas6 group (P<0.05). Thus, Gas6 has potential to be developed as a novel therapeutic agent to treat patients with sepsis and acute lung injury.
    Shock (Augusta, Ga.) 07/2013; · 2.87 Impact Factor
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    ABSTRACT: Forty-eight hour kidney transplantation admissions are a feasible option in selected recipients of live-donor allografts through the use of standardized post-operative protocols, multidisciplinary team patient care, and intensive follow-up at outpatient centers. Age, gender, and pre-transplant dialysis status did not impact the ability to achieve 48-hour admissions. We did not identify any other pre-operative risk factors that contributed to increased length of stay. Although ABO and highly sensitized recipients had longer lengths of stay, the subgroup was too small to achieve statistical significance. We did not encounter any readmissions within the first seven post-operative days. Further improvements in clinical management will enhance the potential to shorten the length of hospital stay for all kidney transplant recipients.
    Clinical Transplantation 06/2013; · 1.49 Impact Factor
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    ABSTRACT: Kidney transplantation is the preferred clinical and most cost-effective option for end-stage renal disease. Significant advances have taken place in the care of the transplant patients with improvements in clinical outcomes. The optimization of the costs of transplantation has been a constant goal as well. We present herein the impact in financial outcomes of a shortened length of stay after kidney transplant.
    International Journal of Angiology 06/2013; 22(2):101-4.
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    ABSTRACT: Pneumatosis intestinalis and portal venous gas are findings usually associated with intra-abdominal surgical catastrophes that frequently require emergent surgical intervention. Herein we present a case of a patient who presented in septic shock, with extensive portal vein gas, diffuse intestinal wall thickening, and atherosclerotic vascular insufficiency in the absence of pneumatosis intestinalis. Given his advanced age, multiple comorbidities, magnitude of the initial findings, and his dramatic clinical response to aggressive fluid resuscitation, a cognitive decision was made to continue with nonoperative management. The patient recovered uneventfully and was discharged home in a stable condition.
    International Journal of Angiology 06/2013; 22(2):123-6.
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    ABSTRACT: Catheterization of the urinary bladder during kidney transplantation is essential. The optimal time to remove the Foley catheter postoperatively is not universally defined. It is our practice to remove the Foley catheter on postoperative day 1 in live donor kidney transplant recipients who meet our standardized protocol criteria. We believe that early removal of Foley catheters increases patient comfort and mobility, decreases the risk of catheter associated urinary tract infections, and allows for decreased hospital length of stay. The hypothetical risk of early removal of Foley catheters would be the increased risk of urine leak. We reviewed 120 consecutive live donor kidney transplant recipients and found that there was not an increased incidence of urine leaks in patients whose Foley catheters were removed on postoperative day 1.
    International Journal of Angiology 03/2013; 22(1):45-8.
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    ABSTRACT: INTRODUCTION: Non-invasive imaging studies can provide visualization of allograft perfusion in the postoperative evaluation of newly transplanted renal allografts. AIM: The purpose of our study was to evaluate the significance of elevated renal artery velocities in the immediate postoperative period. METHODS: Peak systolic velocities (PSVs) were obtained in the transplanted renal artery of 128 patients immediately after transplantation. Repeat allograft Doppler ultrasonography was performed on patients with elevated values. RESULTS: Of the 128 patients, 57 (44.5%) had severely elevated Doppler velocities >400 cm/s on the initial studies. Three patients within this category had persistently elevated values of >400 cm/s, warranting angiographic visualization of the renal vessels. Stent placement within the transplanted renal artery was required in two of these patients. There was normalization of the PSV in the remaining patients. CONCLUSIONS: Routine allograft Doppler ultrasonography in the immediate postoperative period allows for visualization of allograft perfusion. Elevated renal artery velocities in the immediate postoperative period do not necessarily represent stenosis requiring intervention. Failure of the PSV to normalize may require further intervention, and angiography continues to be the gold standard.
    Clinical Transplantation 01/2013; · 1.49 Impact Factor
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    ABSTRACT: The Wnt/β-catenin signaling pathway is well characterized in stem cell biology and plays a critical role in liver development, regeneration, and homeostasis. We hypothesized that pharmacological activation of Wnt signaling protects against hepatic ischemia/reperfusion (I/R) injury through its known proliferative and anti-apoptotic properties. Sprague-Dawley rats underwent 70% hepatic ischemia by microvascular clamping of the hilum of the left and median lobes of the liver for 90 min, followed by reperfusion. Wnt agonist (2-amino-4-[3,4-(methylenedioxy) benzylamino]-6-(3-methoxyphenyl) pyrimidine, 5 mg/kg BW) or vehicle (20% DMSO in saline) in 0.5 ml was injected intraperitoneally (i.p.) 1 h prior to ischemia or infused intravenously over 30 min right after ischemia. Blood and tissue samples from the pre-treated groups were collected 24 h after reperfusion, and a survival study was performed. Hepatic expression of β-catenin and its downstream target gene Axin2 were decreased after I/R while Wnt agonist restored their expression to sham levels. Wnt agonist blunted I/R-induced elevations of AST, ALT, and LDH and significantly improved the microarchitecture of the liver. The cell proliferation determined by Ki67 immunostaining significantly increased with Wnt agonist treatment and inflammatory cascades were dampened in Wnt agonist-treated animals, as demonstrated by attenuations in IL-6, myeloperoxdase, iNOS and nitrotyrosine. Wnt agonist also significantly decreased the amount of apoptosis, as evidenced by decreases in both TUNEL staining as well as caspase-3 activity levels. Finally, the 10-day survival rate was increased from 27% in the vehicle group to 73% in the pre-treated Wnt agonist group and 55% in the Wnt agonist post-ischemia treatment group. Thus, we propose that direct Wnt/β-catenin stimulation may represent a novel therapeutic approach in the treatment of hepatic I/R.
    Shock (Augusta, Ga.) 11/2012; · 2.87 Impact Factor
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    ABSTRACT: The gastrointestinal (GI) syndrome component of acute radiation syndrome (ARS) results from depletion of immature parenchymal stem cells after high dose irradiation and contributes significantly to early mortality. It is associated with severe, irreparable damage in the GI tract and extremely low survival. There is a need for the development of viable mitigators of whole body irradiation (WBI) due to the possibility of unexpected high level radiation exposure from nuclear accidents or attacks. We therefore examined the effect of recombinant human milk fat globule-EGF factor 8 (rhMFG-E8) in mitigating damage after WBI. Male Sprague-Dawley rats were exposed to 10 Gy WBI using Cesium-137 as the radiation source. The animals in the treatment group received rhMFG-E8 (166 µg/kg BW) subcutaneously once a day with the first dose given 6 h after WBI. Blood and tissue samples from the ileum were collected after 3 days of treatment. A separate cohort of animals was treated for 7 days and the 21 day mortality rate was determined. Treatment with rhMFG-E8 significantly improved the survival from 31% to 75% over 21 days. Furthermore, rhMFG-E8 treatment resulted in a 36% reduction in the radiation injury intestinal mucosal damage score, corresponding to visible histological changes. MFG-E8 gene expression was significantly decreased in WBI-induced animals as compared to sham controls. Treatment with rhMFG-E8 increased p53 and p21 expression by 207% and 84% compared to untreated controls. This was accompanied by an 80% increase in the expression of anti-apoptotic cell regulator Bcl-2. p53 and p21 levels correlate with improved survival after radiation injury. These cell regulators arrest the cell after DNA damage and enable DNA repair as well as optimize cell survival. Taken together, these results indicate that rhMFG-E8 ameliorates the GI syndrome and improves survival after WBI by minimizing intestinal cell damage and optimizing recovery.
    PLoS ONE 10/2012; 7(10):e46540. · 3.53 Impact Factor
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    ABSTRACT: Meckel diverticula are remnants of the omphalomesenteric duct. They have 2% incidence in the general population, are usually asymptomatic, and tend to be diagnosed incidentally. The generally held principle had been that asymptomatic cases do not require resection, as exemplified by a 2008 systematic review of over 200 studies. However, a recent series reported an increased risk of malignancies, and recommended mandatory resection. We present a case of Meckel diverticulitis with concurrent infiltrative appendiceal carcinoid in a patient with right lower quadrant pain.
    International Journal of Angiology 09/2012; 21(3):155-8.

Publication Stats

213 Citations
131.82 Total Impact Points


  • 2011–2014
    • Hofstra North Shore-LIJ School of Medicine
      New York City, New York, United States
  • 2009–2013
    • North Shore-Long Island Jewish Health System
      • Department of Surgery
      New York City, New York, United States
    • The Feinstein Institute for Medical Research
      • Center for Immunology and Inflammation
      New York City, NY, United States
  • 2005
    • Staten Island University Hospital
      New York, United States