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Education ?

Medical School Score
New York Institute of Technology (1998)

Affiliations ?

Dr. Steinberg is affiliated with 8 hospitals.

Hospital Affiliations



  • Virtua Memorial Hospital Of Burlington County
    175 Madison Ave, Mount Holly, NJ 08060
    Top 25%
  • St. Mary Medical Center - Langhorne
    1201 Langhorne Newtown Rd, Langhorne, PA 19047
    Top 50%
  • Virtua West Jersey Hospital - Voorhees
    94 Brick Rd, Marlton, NJ 08053
  • Our Lady Of Lourdes Medical Center
    1600 Haddon Ave, Camden, NJ 08103
  • Virtua West Jersey Hospital - Marlton
    94 Brick Rd, Marlton, NJ 08053
  • Lower Bucks Hospital
  • Virtua WJ Hospital Voorhees
  • Virtua WJ Hospital Marlton
  • Publications & Research

    Dr. Steinberg has contributed to 19 publications.
    Title Traumatic Dissection of the Left Anterior Descending Coronary Artery After Blunt Torso Trauma.
    Date September 2010
    Journal The American Surgeon
    Title Prospective Diagnostic Accuracy Assessment of the Hemosil Hs D-dimer to Exclude Pulmonary Embolism in Emergency Department Patients.
    Date June 2010
    Journal Thrombosis Research

    Chest pain and shortness of breath are among the most common symptoms requiring immediate evaluation. Testing for pulmonary embolism (PE) has become easier and widespread due to D-dimer blood tests. Safe use of these tests is only possible if sensitivity is high and they are used in non-high probability patients. We evaluated diagnostic performance of the HemosIL HS D-dimer, which despite FDA approval in 2005, has been minimally reported in prospective standard clinical care.

    Title Effect of Positive End-expiratory Pressure and Tidal Volume on Lung Injury Induced by Alveolar Instability.
    Date May 2007
    Journal Critical Care (london, England)

    INTRODUCTION: One potential mechanism of ventilator-induced lung injury (VILI) is due to shear stresses associated with alveolar instability (recruitment/derecruitment). It has been postulated that the optimal combination of tidal volume (Vt) and positive end-expiratory pressure (PEEP) stabilizes alveoli, thus diminishing recruitment/derecruitment and reducing VILI. In this study we directly visualized the effect of Vt and PEEP on alveolar mechanics and correlated alveolar stability with lung injury. METHODS: In vivo microscopy was utilized in a surfactant deactivation porcine ARDS model to observe the effects of Vt and PEEP on alveolar mechanics. In phase I (n = 3), nine combinations of Vt and PEEP were evaluated to determine which combination resulted in the most and least alveolar instability. In phase II (n = 6), data from phase I were utilized to separate animals into two groups based on the combination of Vt and PEEP that caused the most alveolar stability (high Vt [15 cc/kg] plus low PEEP [5 cmH2O]) and least alveolar stability (low Vt [6 cc/kg] and plus PEEP [20 cmH2O]). The animals were ventilated for three hours following lung injury, with in vivo alveolar stability measured and VILI assessed by lung function, blood gases, morphometrically, and by changes in inflammatory mediators. RESULTS: High Vt/low PEEP resulted in the most alveolar instability and lung injury, as indicated by lung function and morphometric analysis of lung tissue. Low Vt/high PEEP stabilized alveoli, improved oxygenation, and reduced lung injury. There were no significant differences between groups in plasma or bronchoalveolar lavage cytokines or proteases. CONCLUSION: A ventilatory strategy employing high Vt and low PEEP causes alveolar instability, and to our knowledge this is the first study to confirm this finding by direct visualization. These studies demonstrate that low Vt and high PEEP work synergistically to stabilize alveoli, although increased PEEP is more effective at stabilizing alveoli than reduced Vt. In this animal model of ARDS, alveolar instability results in lung injury (VILI) with minimal changes in plasma and bronchoalveolar lavage cytokines and proteases. This suggests that the mechanism of lung injury in the high Vt/low PEEP group was mechanical, not inflammatory in nature.

    Title Chemically Modified Tetracycline (col-3) Improves Survival if Given 12 but Not 24 Hours After Cecal Ligation and Puncture.
    Date January 2007
    Journal Shock (augusta, Ga.)

    Sepsis can result in excessive and maladaptive inflammation that is responsible for more than 215,00 deaths per year in the United State alone. Current strategies for reducing the morbidity and mortality associated with sepsis rely on treatment of the syndrome rather than prophylaxis. We have been investigating a modified tetracycline, COL-3, which can be given prophylactically to patients at high risk for developing sepsis. Our group has shown that COL-3 is very effect at preventing the sequelae of sepsis if given before or immediately after injury in both rat and porcine sepsis models. In this study, we wanted to determine the "treatment window" for COL-3 after injury at which it remains protective. Sepsis was induced by cecal ligation and puncture (CLP). Rats were anesthetized and placed into five groups: CLP (n = 20) = CLP without COL-3, sham (n = 5) = surgery without CLP or COL-3, COL3@6h (n = 10) = COL-3 given by gavage 6 h after CLP, COL3@12h (n = 10) = COL-3 given by gavage 12 h after CLP, and COL3@24h (n = 20) = COL-3 given by gavage 24 h after CLP. COL-3 that was given at 6 and 12 h after CLP significantly improved survival as compared with the CLP and the CLP@24h groups. Improved survival was associated with a significant improvement in lung pathology assessed morphologically. These data suggest that COL-3 can be given up to 12 h after trauma and remain effective.

    Title Chemically Modified Tetracycline Improves Contractility in Porcine Coronary Ischemia/reperfusion Injury.
    Date October 2006
    Journal Journal of Cardiac Surgery

    BACKGROUND: Reperfusion of ischemic myocardium has been implicated in extension of infarct size and deleterious clinical outcomes. Anti-inflammatory agents reduce this reperfusion injury. Chemically modified tetracycline-3 (CMT-3) (Collagenex Pharmaceuticals, Newtown, PA, USA) lacks antimicrobial properties yet retains anti-inflammatory activity. We examined infarct size and myocardial function in a porcine coronary artery occlusion/reperfusion model in CMT-3-treated and control animals. METHODS: Yorkshire pigs (n = 8) underwent median sternotomy, pretreatment with heparin (300 U/kg and 67 U/kg/hr IV) and lidocaine (1 mg/kg IV) and were divided into two groups. Group one (n = 4) had the left anterior descending artery (LAD) occluded for 1 hour, after which it was reperfused for 2 hours. Group two (n = 4) had an identical protocol to group one except CMT-3 (2 mg/kg IV) was administered prior to occlusion of the LAD. RESULTS: Animals receiving CMT-3 had significantly decreased infarct size in relation to the ventricular area-at-risk (AAR) (28 +/- 9% vs. 64 +/- 8%; p < 0.05). Myocardial contractile function was superior in the CMT-3 treatment, indicated by a higher cardiac index (2.9 +/- 0.3 vs. 2.0 +/- 0.3 L/min/m(2); p < 0.05) and stroke volume index (22 +/- 2 vs. 17 +/- 1 L/m(2)/beat; p < 0.05). CONCLUSIONS: CMT-3 decreased infarct size in relation to the AAR resulting in relative preservation of contractility, suggesting CMT-3 may improve outcomes during myocardial ischemia reperfusion.

    Title Wood Smoke Inhalation Causes Alveolar Instability in a Dose-dependent Fashion.
    Date November 2005
    Journal Respiratory Care

    BACKGROUND: Wood smoke inhalation causes severe ventilation and oxygenation abnormalities. We hypothesized that smoke inhalation would cause lung injury by 2 mechanisms: (1) direct tissue injury by the toxic chemicals in the smoke and (2) a mechanical shear-stress injury caused by alveolar instability (ie, alveolar recruitment/derecruitment). We further postulated that alveolar instability would increase with the size of the cumulative smoke dose. METHODS: Anesthetized pigs were ventilated and instrumented for hemodynamic and blood-gas measurements. After baseline readings, the pigs were exposed to 5 separate doses of wood smoke, each dose lasting 1 min. Factors studied included hemodynamics, pulmonary variables, and in vivo photomicroscopy of alveolar mechanics (ie, the dynamic change in alveolar size with ventilation). RESULTS: Smoke inhalation significantly increased alveolar instability with 4 min and 5 min of smoke exposure. Significant rises in carboxyhemoglobin levels and in pulmonary shunt were also observed at 4 min and 5 min of smoke exposure. Lung histology demonstrated severe damage characteristic of acute lung injury. CONCLUSIONS: We demonstrated that wood smoke inhalation causes alveolar instability and that instability increases with each dose of smoke. These data suggest that smoke inhalation may cause a "2-hit" insult: the "first hit" being a direct toxic injury and the "second hit" being a shear-stress injury secondary to alveolar instability.

    Title Alveolar Instability Causes Early Ventilator-induced Lung Injury Independent of Neutrophils.
    Date January 2004
    Journal American Journal of Respiratory and Critical Care Medicine

    Intratracheal instillation of Tween causes a heterogeneous surfactant deactivation in the lung, with areas of unstable alveoli directly adjacent to normal stable alveoli. We employed in vivo video microscopy to directly assess alveolar stability in normal and surfactant-deactivated lung and tested our hypothesis that alveolar instability causes a mechanical injury, initiating an inflammatory response that results in a secondary neutrophil-mediated proteolytic injury. Pigs were mechanically ventilated (VT 10 cc/kg, positive end-expiratory pressure [PEEP] 3 cm H2O), randomized to into three groups, and followed for 4 hours: Control group (n = 3) surgery only; Tween group (n = 4) subjected to intratracheal Tween (surfactant deactivator causing alveolar instability); and Tween + PEEP group (n = 4) subjected to Tween with increased PEEP (15 cm H2O) to stabilize alveoli. The magnitude of alveolar instability was quantified by computer image analysis. Surfactant-deactivated lungs developed significant histopathology only in lung areas with unstable alveoli without an increase in neutrophil-derived proteases. PEEP stabilized alveoli and significantly reduced histologic evidence of lung injury. Thus, in this model, alveolar instability can independently cause ventilator-induced lung injury. To our knowledge, this is the first study to directly confirm that unstable alveoli are subjected to ventilator-induced lung injury whereas stable alveoli are not.

    Title Chlamydia Trachomatis Infections in Female Soldiers, Israel.
    Date January 2004
    Journal Emerging Infectious Diseases
    Title Stabilization of Post-trabeculectomy Flat Anterior Chamber with Healon and Sulfur Hexafluoride.
    Date December 2003
    Journal Journal of Cataract and Refractive Surgery

    We present the management of 2 cases of post-trabeculectomy flat anterior chamber with hypotony due to an overflowing fistula. When separate attempts to reform the anterior chamber by intracameral injection of sulfur hexafluoride (SF(6)) and sodium hyaluronate 1.0% (Healon) failed, we injected SF(6) 100% with Healon into the anterior chamber. This stabilized the anterior chamber without compromising the integrity of the filtering bleb. No complications were observed. This simple, safe, and effective procedure offers another option for the management of a flat anterior chamber due to overfiltration.

    Title Prickly Pear Fruit Bezoar Presenting As Rectal Perforation in an Elderly Patient.
    Date November 2003
    Journal International Journal of Colorectal Disease

    BACKGROUND AND AIMS: Prickly pear fruit rectal seed bezoars are an extremely rare entity. Only nine cases of rectal seed bezoar have been reported, only one of which involved the prickly pear fruit seed. Furthermore, to our knowledge, this is also the first reported case presenting as rectal perforation. PATIENTS AND METHODS: We report a case of prickly pear fruit bezoar occurring in the elderly whom presented with rectal perforation. Consistent with physical signs, laboratory results, and radiological findings the patient was diagnosed with acute perforation of the rectum. A Hartman procedure was performed, and a colostomy was placed. RESULTS: Currently there are very few data regarding seed bezoars reaching the rectum. There are even fewer data concerning this occurrence in the elderly, and the literature contains no report of this phenomenon presenting or even progressing into perforation. We report this rare entity to the existing literature. CONCLUSION: We report a rare but important case. A prickly pear fruit phytobezoar presenting as rectal perforation. This case may add to the increasing awareness of the danger associated with ingestion of certain foodstuffs. The previously benign sunflower and psyllium seeds are now known to cause bezoar. We feel that the prickly pear fruit should join this small but important list.

    Title Positive End-expiratory Pressure After a Recruitment Maneuver Prevents Both Alveolar Collapse and Recruitment/derecruitment.
    Date July 2003
    Journal American Journal of Respiratory and Critical Care Medicine

    We tested the hypothesis that collapsed alveoli opened by a recruitment maneuver would be unstable or recollapse without adequate positive end-expiratory pressure (PEEP) after recruitment. Surfactant deactivation was induced in pigs by Tween instillation. An in vivo microscope was placed on a lung area with significant atelectasis and the following parameters measured: (1) the number of alveoli per field and (2) alveolar stability (i.e., the change in alveolar size from peak inspiration to end expiration). We previously demonstrated that unstable alveoli cause lung injury. A recruitment maneuver (peak pressure = 45 cm H2O, PEEP = 35 cm H2O for 1 minute) was applied and alveolar number and stability were measured. Pigs were then separated into two groups with standard ventilation plus (1) 5 PEEP or (2) 10 PEEP and alveolar number and stability were again measured. The recruitment maneuver opened a significant number of alveoli, which were stable during the recruitment maneuver. Although both 5 PEEP and 10 PEEP after recruitment demonstrated improved oxygenation, alveoli ventilated with 10 PEEP were stable, whereas alveoli ventilated with 5 PEEP showed significant instability. This suggests recruitment followed by inadequate PEEP permits unstable alveoli and may result in ventilator-induced lung injury despite improved oxygenation.

    Title Is There a Need for Taking Blood Cultures from Febrile Adults Discharged from the Emergency Department?
    Date June 2003
    Journal The Journal of Infection
    Title Reoccurrence of Culture-positive Pertussis in an Infant Initially Treated with Azithromycin and Steroids.
    Date November 2002
    Journal Archives of Pediatrics & Adolescent Medicine
    Title Alveolar Mechanics Alter Hypoxic Pulmonary Vasoconstriction.
    Date July 2002
    Journal Critical Care Medicine

    OBJECTIVES: Hypoxic pulmonary vasoconstriction is the primary physiologic mechanism that maintains a proper ventilation/perfusion match, but it fails in diffuse lung injuries such as acute respiratory distress syndrome. Acute respiratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics (i.e., dynamic change in alveolar size and shape during ventilation), converting normal stable alveoli into unstable alveoli. We hypothesized that alveolar instability stents open pulmonary microvessels and is the mechanism of hypoxic pulmonary vasoconstriction failure associated with acute respiratory distress syndrome. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Anesthetized ventilated pigs were prepared surgically for hemodynamic monitoring and were subjected to a right thoracotomy. An in vivo microscope was attached to the right lung, and the microvascular response to hypoxia (F(IO(2)), 15%) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by surfactant deactivation (Tween lavage). MEASUREMENTS AND MAIN RESULTS: Alveolar instability, defined as the difference between alveolar area at peak inspiration and end expiration and assessed as a percentage change (I-E Delta%), was significantly increased after Tween (23.9 +/- 3.0, I-E Delta%) compared with baseline (2.4 +/- 1.0, I-E Delta%). Alveolar instability was associated with the following microvascular changes: a) increased vasoconstriction (Tween, 14.9 +/- 1.0%) in response to hypoxia compared with baseline (10.8 +/- 1.2%, p <.05); and b) increased mean vascular diameter (Tween, 41.2 +/- 1.5 microm) compared with the mean diameter at baseline (24.6 +/- 1.0 microm, p <.05). CONCLUSION: Unstable alveoli stent open pulmonary vessels, which may explain the failure of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.

    Title Visual Validation of the Mechanical Stabilizing Effects of Positive End-expiratory Pressure at the Alveolar Level.
    Date August 2001
    Journal The Journal of Surgical Research

    BACKGROUND: Positive end-expiratory pressure (PEEP) reduces ventilator-induced lung injury (VILI), presumably by mechanically stabilizing alveoli and decreasing intrapulmonary shear. Although there is indirect support for this concept in the literature, direct evidence is lacking. In a surfactant depletion model of acute lung injury we observed unstable alveolar mechanics referred to as repeated alveolar collapse and expansion (RACE) as measured by changes in alveolar area from inspiration to expiration (I - E(Delta)). We tested the hypothesis that over a range of tidal volumes PEEP would prevent RACE by mechanically stabilizing alveoli. MATERIALS AND METHODS: Yorkshire pigs were randomized to three groups: control (n = 4), Tween (surfactant-deactivating detergent) (n = 4), and Tween + PEEP (7 cm H(2)O) (n = 4). Using in vivo video microscopy individual alveolar areas were measured with computer image analysis at end inspiration and expiration over consecutive increases in tidal volume (7, 10, 15, 20, and 30 cc/kg.) I - E(Delta) was calculated for each alveolus. RESULTS: Surfactant deactivation significantly increased I - E(Delta) at every tidal volume compared to controls (P < 0.05). PEEP prevented this change, returning I - E(Delta) to control levels over a spectrum of tidal volumes. CONCLUSIONS: RACE occurs in our surfactant deactivation model of acute lung injury. PEEP mechanically stabilizes alveoli and prevents RACE over a range of tidal volumes. This is the first study to visually document the existence of RACE and the mechanical stabilizing effects of PEEP at the alveolar level. The ability of PEEP to stabilize alveoli and reduce shear during mechanical ventilation has important implications for therapeutic strategies directed at VILI and acute respiratory distress syndrome.

    Title Altered Alveolar Mechanics in the Acutely Injured Lung.
    Date June 2001
    Journal Critical Care Medicine

    OBJECTIVES: Alterations in alveolar mechanics (i.e., the dynamic change in alveolar size during tidal ventilation) are thought to play a critical role in acute lung injuries such as acute respiratory distress syndrome (ARDS). In this study, we describe and quantify the dynamic changes in alveolar mechanics of individual alveoli in a porcine ARDS model by direct visualization using in vivo microscopy. DESIGN: Prospective, observational, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Pigs were anesthetized and placed on mechanical ventilation, underwent a left thoracotomy, and were separated into the following two groups post hoc: a control group of instrumented animals with no lung injury (n = 5), and a lung injury group in which lung injury was induced by tracheal Tween instillation, causing surfactant deactivation (n = 5). Pulmonary and systemic hemodynamics, blood gases, lung pressures, subpleural blood flow (laser Doppler), and alveolar mechanics (in vivo microscopy) were measured in both groups. Alveolar size was measured at peak inspiration (I) and end expiration (E) on individual subpleural alveoli by image analysis. Histologic sections of lung tissue were taken at necropsy from the injury group. MEASUREMENTS AND MAIN RESULTS: In the acutely injured lung, three distinct alveolar inflation-deflation patterns were observed and classified: type I alveoli (n = 37) changed size minimally (I - EDelta = 367 +/- 88 microm2) during tidal ventilation; type II alveoli (n = 37) changed size dramatically (I - EDelta = 9326 +/- 1010 microm2) with tidal ventilation but did not totally collapse at end expiration; and type III alveoli (n = 12) demonstrated an even greater size change than did type II alveoli (I - EDelta = 15,418 +/- 1995 microm2), and were distinguished from type II in that they totally collapsed at end expiration (atelectasis) and reinflated during inspiration. We have termed the abnormal alveolar inflation pattern of type II and III alveoli "repetitive alveolar collapse and expansion" (RACE). RACE describes all alveoli that visibly change volume with ventilation, regardless of whether these alveoli collapse totally (type III) at end expiration. Thus, the term "collapse" in RACE refers to a visibly obvious collapse of the alveolus during expiration, whether this collapse is total or partial. In the normal lung, all alveoli measured exhibited type I mechanics. Alveoli were significantly larger at peak inspiration in type II (18,266 +/- 1317 microm2, n = 37) and III (15,418 +/- 1995 microm2, n = 12) alveoli as compared with type I (8214 +/- 655 microm2, n = 37). Tween caused a heterogenous lung injury with areas of normal alveolar mechanics adjacent to areas of abnormal alveolar mechanics. Subsequent histologic sections from normal areas exhibited no pathology, whereas lung tissue from areas with RACE mechanics demonstrated alveolar collapse, atelectasis, and leukocyte infiltration. CONCLUSION: Alveolar mechanics are altered in the acutely injured lung as demonstrated by the development of alveolar instability (RACE) and the increase in alveolar size at peak inspiration. Alveolar instability varied from alveolus to alveolus in the same microscopic field and included alveoli that changed area greatly with tidal ventilation but remained patent at end expiration and those that totally collapsed and reexpanded with each breath. Thus, alterations in alveolar mechanics in the acutely injured lung are complex, and attempts to assess what may be occurring at the alveolar level from analysis of inflection points on the whole-lung pressure/volume curve are likely to be erroneous. We speculate that the mechanism of ventilator-induced lung injury may involve altered alveolar mechanics, specifically RACE and alveolar overdistension.

    Title Successful Human in Vitro Fertilization Using a Modified Human Tubal Fluid Medium Lacking Glucose and Phosphate Ions.
    Date April 1995
    Journal Fertility and Sterility

    OBJECTIVE: To determine the effect of medium with or without glucose and phosphate on the fertilization and development of human oocytes. DESIGN: Sequential allocation of alternate patients to one of two treatment groups. SETTING: Private practice infertility programs. PATIENTS: Ten couples requesting treatment for infertility. INTERVENTIONS: Gametes from each couple were collected, washed, and incubated in one of two culture media under investigation. MAIN OUTCOME MEASURES: Number of oocytes collected, fertilized, cleaving, replaced, and implanting in each patient. Development of any supernumerary embryos to fully expanded blastocysts in vitro. RESULTS: There was a significant increase in the proportion of transferred embryos implanting in the group of patients whose gametes were handled in medium devoid of glucose and phosphate. All other comparisons of factors that may have influenced implantation rates between the two groups of patients were not significantly different. CONCLUSIONS: High rates of fertilization, cleavage, implantation, and development of supernumerary human embryos to the blastocyst stage in vitro were obtained with a modified human tubal fluid medium containing ethylenediaminetetraacetic acid and glutamine but devoid of glucose and phosphate ions. A prospective randomized trial is necessary to evaluate the clinical significance of these observations.

    Title Functional Homology Between N-myc and C-myc in Murine Plasmacytomagenesis: Plasmacytoma Development in N-myc Transgenic Mice.
    Date July 1992
    Journal Oncogene

    Mouse plasmacytomas induced by pristane oil alone, or in combination with Abelson murine leukemia virus (A-MuLV), regularly carry one of three alternative chromosomal translocations that juxtapose c-myc to immunoglobulin heavy- or light-chain loci. E mu-c-myc transgenic mice develop translocation-free plasmacytomas after induction by pristane oil and/or A-MuLV [Sugiyama, H., Silva, S., Wang, Y., Weber, G., Babonits, M., Rosen, A., Wiener, F. & Klein, G. (1990). Int. J. Cancer, 46, 845-852]. In order to test whether another member of the myc family, N-myc, could play a similar role as c-myc, we treated E mu-N-myc transgenic mice with pristane and helper-free A-MuLV. Of 20 mice that received a single pristane injection followed by A-MuLV, 17 developed plasmacytomas with a mean latency period of 54 +/- 20 days. In a corresponding group that only received a single pristane injection, five out of six transgenic mice developed plasmacytomas with a mean latency period of 142 +/- 32 days. However, after three monthly injections of pristane, all 15 transgenic mice developed plasmacytomas with a mean latency period of 128 +/- 20 days. All plasmacytomas expressed the N-myc transgene, while none of them expressed either c-myc or endogenous N-myc. None of the tumors carried the usual plasmacytoma-associated translocations.

    Title Meningeal Melanocytoma with Invasion of the Thoracic Spinal Cord. Case Report.
    Date June 1978
    Journal Journal of Neurosurgery

    A case is presented of meningeal melanocytoma that invaded the thoracic spinal cord of a 71-year-old woman. The light and electron microscopic features of the lesion indicate that it derives from melanocytes normally found in the leptomeninges. This tumor closely resembles the dermal cellular blue nevus and does not have the ultrastructure of a meningioma. "Melanotic meningioma" is consequently a misnomer and the name "meningeal melanocytoma" is more appropriate. These tumors may appear to be benign histologically, but they are locally aggressive. Total surgical excision offers the best chance for cure.

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