R H Turnage

Louisiana State University Health Sciences Center New Orleans, Baton Rouge, LA, United States

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Publications (82)218.32 Total impact

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    ABSTRACT: Fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) has proven to be a valuable tool in the initial diagnosis, staging, and restaging of a variety of cancers. The potential use of FDG-PET in the evaluation and management of hepatocellular carcinoma (HCC) continues to evolve. The purpose of this study was to investigate the effectiveness of FDG-PET for the detection and staging of HCC. In addition, we also assessed the correlation between FDG-PET positivity, tumor size, a-fetal protein level (AFP), and histologic grade. All patients on the hepatobiliary and liver transplant service with biopsy proven HCC that underwent FDG-PET between January 2000 and December 2004 were selected for a retrospective review. Results of the FDG-PET scan were compared with other imaging studies [computed tomography (CT), magnetic resonance imaging (MRI), ultrasonography], intraoperative findings, tumor size, AFP levels, and histologic grade. Of the 20 patients who underwent 18F-FDG PET, increased FDG uptake was noted in 14 scans (70%). These 20 patients fell into 2 groups: 1 for detecting HCC (Group A) and 1 for staging HCC (Group B). There were 7 patients in Group A; only 2 scans (28.6%) showed increased uptake. There were 13 patients in Group B; 12 scans (92.3%) showed increased uptake. In Group B, 11 of the 13 scans (84.6%) provided an accurate representation of the disease process. Two scans failed to accurately portray the disease; one scan failed to show any increase in uptake, and the other scan failed to detect positive nodes that were found during surgery. FDG-PET detected only 2 of 8 tumors (25%) < or = 5 cm in size. All 12 PET scans (100%) in tumors > or = 5 cm and/or multiple in number were detected by FDG-PET. FDG-PET scans with AFP levels < 100 ng/ml were positive in 5 of 9 patients (55.6%). In patients with levels > 100 ng/ml, 6 of 7 patients (85.7%) had positive scans. Histologically, there were 6 well-differentiated, 6 moderately differentiated, and 2 poorly differentiated HCCs. FDG-PET detected 4 of 6 for both well- and moderately differentiated HCCs. Both poorly differentiated HCCs were detected. The intensity was evenly distributed between the different histologic grades. There was a strong correlation of FDG uptake with tumor size. There were 5 HCCs with primary tumors >10 cm in size; 4 showed intense uptake on the scan. In contrast, of the 8 tumors < or = 5 cm in size, 6 were negative for uptake. The sensitivity of FDG-PET in detecting HCC < or = 5 cm in size is low and therefore may not be helpful in detecting all of these tumors. For larger tumors, there is a strong correlation of sensitivity and uptake intensity with tumor size and elevated AFP levels. FDG-PET sensitivity and uptake intensity did not correlate with histologic grade. In the setting of extrahepatic disease, FDG-PET seems to be an effective accurate method for HCC staging; however, whether PET offers any benefit over traditional imaging has yet to be determined.
    International surgery 01/2010; 95(1):67-75. · 0.31 Impact Factor
  • F Dean Griffen, Richard H Turnage
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    ABSTRACT: Closed claims reviews are a robust source of severe surgical errors for study. Most errors are preventable. Most preventable technical errors and judgment errors occur during care provided by competent surgeons. Failure to operate within a proper scope-of-practice is the most common cause of incompetence. Patient factors and systems failures, including human factors, cause or profoundly contribute to the cause of most technical errors. Regardless of its cause or preventability, a technical error sets the stage for other errors in care that relate to systems' failures and surgeons' judgment failures. Failed judgment and poor decision-making are usually the result of cognitive errors caused by flawed behavioral practices instead of lack of knowledge. Systems of care and good behavioral practices are catalysts that maximize the power of knowledge and skill to achieve good outcomes. The uniform application of knowledge and skill in a favorable environment is as important as the possession of knowledge and skill. Identifying systems and behavioral causes of errors may help to define best practices and lead to safer patient care through improved systems of care and increased diligent attention to ordinary tasks that require more time than knowledge on the part of surgeons.
    Advances in Surgery 01/2009; 43:199-209.
  • Journal of Surgical Research - J SURG RES. 01/2008; 144(2):353-353.
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    ABSTRACT: CXCR4 is a chemokine receptor that has recently been implicated to play a pivotal role in breast cancer growth and metastasis. In animal models, reduction of CXCR4 expression significantly abrogated metastatic disease and prolonged survival. In human breast cancers, CXCR4 overexpression may portend a worse clinical course. Recent data suggest that HER-2 up-regulates CXCR4, but whether this is applicable in the clinical setting is not known. In this study, we evaluated the role of CXCR4 overexpression in breast cancer and determined whether it can serve as a potential marker of tumor recurrence in HER-2 negative tumors. One hundred three patients with stages I to III breast cancers and 6 benign breast tissues were prospectively accrued and analyzed. Study homogeneity was maintained by standardized treatment, surveillance, and compliance protocols. CXCR4 levels were detected using Western blots and results were quantified against 1 microg of HeLa cells (positive controls). HER-2 expression was evaluated using the Hercep program, (Dako Corp., Carpinteria, CA) with a positive result defined as > or = 2. CXCR4 expression was defined as low (<6.6-fold) or high (> or = 6.6-fold). Primary endpoints were cancer recurrence and death. Statistical analysis performed included Spearman's correlation, independent samples t-test, Kaplan-Meier survival analysis, and log-rank test. All 103 cancer specimens had CXCR4 overexpression (mean 6.6 +/- 4.7), while none of the 6 benign breast tissues had detectable level of CXCR4. There were 36 HER-2 (+) tumors and 67 HER-2 (-) tumors. There was no statistical significance in mean CXCR4 overexpression between HER-2 (+) [5.6] and HER-2 (-) [6.6] cancers (P = 0.3; independent samples t-test). Recurrences occurred in 18 of 103 patients (17%); 10 occurred in HER-2 (+) tumors, and 8 occurred in HER-2 (-) patients. CXCR4 expression level was not predictive of cancer recurrence (P = 0.80) or overall survival (P = 0.70) in the HER-2 (+) group. However, among HER-2 negative tumors, 7 of 8 recurrences occurred in the high CXCR4 group (P = 0.037). There was no correlation between the degree of CXCR4 overexpression with tumor size (r = 0.13, P = 0.22), nodal status (r = 0.019, P = 0.4), ER/PR status (r = 0.12, P = 0.29), and HER-2 status (r = 0.091, P = 0.36). CXCR4 overexpression was observed in all 103 breast cancer specimens but was undetectable in benign breast tissues. CXCR4 overexpression does not correlate with tumor size, nodal status, ER/PR status, and HER-2 status. High CXCR4 overexpression had a significant impact on disease-free survival in HER-2 negative breast cancer patients and may help identify a subset of HER-2 negative breast cancers that have a more aggressive biological behavior.
    Journal of Surgical Research 08/2007; 141(1):53-9. · 2.02 Impact Factor
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    ABSTRACT: The role of whole-body fluorine-18-FDG positron emission tomography (FDG-PET) as an adjunct localize recurrence in stages II and III breast cancer patients who present with clinical suspicion for recurrence is not well established. We report our experience in such a patient population. A retrospective review of all patients with stages II and III breast cancer who had a whole-body FDG-PET scan was performed. Of the 23 patients who fit the criteria, 9 had stage II and 14 had stage III breast cancer. Overall sensitivity, specificity, and accuracy were 81%, 100%, and 87%, respectively. Positive and negative predictive values for stages II and III were 100% and 83%, respectively, and 100% and 50%, respectively. FDG-PET detected two recurrences that were missed by conventional imagings, but such recurrences were local and amenable for biopsy. In patients with stages II and III breast cancer who present with a suspicion for recurrent disease, a whole-body FDG-PET scan may be a useful adjunct in the evaluation of recurrence. However, its added benefit over conventional imaging should be questioned.
    World Journal of Surgery 09/2006; 30(8):1422-7. · 2.23 Impact Factor
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    ABSTRACT: In a prospective trial, to determine if eIF4E overexpression in breast cancer specimens is correlated with VEGF elevation, increased tumor microvessel density (MVD) counts, and a worse clinical outcome irrespective of nodal status. In vitro, the overexpression of eukaryotic initiation factor 4E (eIF4E) up-regulates the translation of mRNAs with long 5'-untranslated regions (5'-UTRs). One such gene product is the vascular endothelial growth factor (VEGF). A total of 114 stage I to III breast cancer patients were prospectively accrued and followed with a standardized clinical surveillance protocol. Cancer specimens were quantified for eIF4E, VEGF, and MVD. Outcome endpoints were cancer recurrence and cancer-related death. eIF4E overexpression was found in all cancer specimens (mean +/- SD, 12.5 +/- 7.6-fold). Increasing eIF4E overexpression correlated with increasing VEGF elevation (r = 0.24, P = 0.01, Spearman's coefficient), and increasing MVD counts (r = 0.35, P < 0.0002). Patients whose tumor had high eIF4E overexpression had shorter disease-free survival (P = 0.004, log-rank test) and higher cancer-related deaths (P = 0.002) than patients whose tumors had low eIF4E overexpression. Patients with high eIF4E had a hazard ratio for cancer recurrence and cancer-related death of 1.8 and 2.1 times that of patients with low eIF4E (respectively, P = 0.009 and P = 0.002, Cox proportional hazard model). In breast cancer patients, increasing eIF4E overexpression in the cancer specimens correlates with higher VEGF levels and MVD counts. Patients whose tumors had high eIF4E overexpression had a worse clinical outcome, independent of nodal status. Thus, eIF4E overexpression in breast cancer appears to predict increased tumor vascularity and perhaps cancer dissemination by hematogenous means.
    Annals of Surgery 05/2006; 243(5):684-90; discussion 691-2. · 6.33 Impact Factor
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    ABSTRACT: An incidental finding of focal thyroid uptake (thyroid incidentaloma) from an 18F-fluorodeoxyglucose positron emission tomography (PET) positron presents a diagnostic challenge. We evaluated the incidence of thyroid incidentaloma identified by PET scans and the likelihood of malignancy associated with this finding. Records from all patients from January 1, 2000 to November 30, 2003 who had focal thyroid uptake without any history of thyroid disease were culled. Of the 6241 PET scans performed, focal thyroid uptake was observed in 76 patients (1.2%). Only 14 patients (18%) underwent biopsy. Four of 14 patients (28.6%) had papillary thyroid carcinoma, 7 (50%) had hyperplasia, and 1 each had thyroiditis, nodular goiter, and follicular neoplasm. The incidence of PET thyroid incidentalomas was 1.2 per cent and the incidence of malignancy was 28.6 per cent. Given the high likelihood of malignancy, a further diagnostic workup for surgically fit patients is warranted.
    The American surgeon 04/2006; 72(3):272-5. · 0.92 Impact Factor
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    ABSTRACT: The rigorous maintenance of normoglycemia by the administration of insulin is beneficial to critically ill patients. Because insulin induces endothelial nitric oxide (NO) release, and the constitutive release of NO maintains normal microvascular permeability, the authors postulated that insulin would prevent peroxide (H(2)O(2))-induced endothelial barrier dysfunction, an effect dependent on endothelial NO synthase (eNOS) activity. Murine lung microvascular endothelial cells (LMEC) grown to confluence on 8 micro pore polyethylene filters were exposed to media (control), H(2)O(2) (20 to 500 micromol/L), insulin (1 to 1,000 nmol/L) or insulin (100 nmol/L) + H(2)O(2) (10(-4)mol/L). Endothelial monolayer permeability was quantitated by measuring the transendothelial electrical resistance at 15-minute intervals for 120 minutes. Other cells were exposed to H(2)O(2) and insulin after pretreatment with a NO scavenger (PTIO), an eNOS inhibitor (L-NIO), or a phosphoinositol-3-kinase inhibitor (LY-294002). H(2)O(2) caused a concentration- and time-dependent reduction in electrical resistance consistent with an increase in monolayer permeability. This effect was prevented by insulin. Inhibiting NO release (L-NIO, LY-294002) or scavenging NO (PTIO) abolished this protective effect. These data suggest that insulin may modulate endothelial barrier function during oxidant stress by inducing the release of NO.
    Surgery 02/2006; 139(1):82-91. · 3.37 Impact Factor
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    ABSTRACT: Oxidant-mediated modulation of the intracellular redox state affects the apoptotic cascade by altering the balance between cellular signals for survival and suicide. Apolipoprotein A-IV (Apo A-IV) is known to possess antioxidant-like activity. In the present study, we tested 1) whether Apo A-IV could influence redox-dependent apoptosis and, if so, 2) whether such an effect could be mediated by modulation of intracellular redox balance. Mitotic competent, undifferentiated PC-12 cells were incubated with either tert-butyl hydroperoxide (TBH) or diamide with or without preincubation with human Apo A-IV. Apo A-IV significantly decreased apoptosis produced by both TBH and diamide, and washout of A-IV before incubation with TBH and diamide did not eliminate its protective effect. Apo A-I had no such protective effect. The Apo A-IV effect was not blocked by D,L-buthionine-[S,R]-sulfoximine, but it was reversed by both dehydroisoandrosterone and transfection with an antisense oligodeoxynucleotide to glucose-6-phosphate dehydrogenase (G6PD). Apo A-IV abolished the transient, oxidant-induced rise in glutathione disulfide (GSSG) and cellular redox imbalance previously shown to initiate the apoptotic cascade. Apo A-IV had no effect on GSSG reductase activity, but it stimulated G6PD activity 10-fold. These results suggest a novel role for Apo A-IV in the regulation of intracellular glutathione redox balance and the modulation of redox-dependent apoptosis via stimulation of G6PD activity.
    AJP Cell Physiology 02/2006; 290(1):C95-C103. · 3.71 Impact Factor
  • Journal of Surgical Research - J SURG RES. 01/2006; 130(2):218-219.
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    ABSTRACT: A previous study of patients with stage I to III breast cancer showed that those patients whose tumors were in the highest tertile of eIF4E overexpression experienced a higher risk for recurrence. This study was designed to determine whether high eIF4E overexpression predicts cancer recurrence independent of nodal status by specifically targeting patients with node-positive disease. The prospective trial was designed to accrue 168 patients with node-positive breast cancer to detect a 2.5-fold increase in risk for recurrence. eIF4E level was quantified by Western blots as x-fold elevated compared with breast tissues from noncancer patients. End points measured were disease recurrence and cancer-related death. Statistical analyses performed include survival analysis by the Kaplan-Meier method, log-rank test, and Cox proportional hazard model. One hundred seventy-four patients with node-positive breast cancer were accrued. All patients fulfilled study inclusion and exclusion criteria, treatment protocol, and surveillance requirements, with a compliance rate >95%. The mean eIF4E elevation was 11.0 +/- 7.0-fold (range, 1.4-34.3-fold). Based on previously published data, tertile distribution was as follow: 1) lowest tertile (<7.5-fold) = 67 patients, 2) intermediate tertile (7.5-14-fold) = 54 patients, and 3) highest tertile (>14-fold) = 53 patients. At a median follow up of 32 months, patients with the highest tertile had a statistically significant higher cancer recurrence rate (log-rank test, P = 0.002) and cancer-related death rate (P = 0.036) than the lowest group. Relative risk calculations demonstrated that high eIF4E patients had a 2.4-fold increase in relative risk increase for cancer recurrence (95% confidence interval, 1.2-4.1; P = 0.01). In this prospective study designed to specifically address risk for recurrence in patients with node-positive breast cancer, the patients whose tumors were in the highest tertile of eIF4E overexpression had a 2.4-fold increase in relative risk for cancer recurrence. Therefore, eIF4E overexpression appears to be an independent predictor of a worse outcome in patients with breast cancer independent of nodal status.
    Annals of Surgery 10/2005; 242(4):584-90; discussion 590-2. · 6.33 Impact Factor
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    ABSTRACT: The roles of individual types of cerebral cells in contributing to brain edema are undefined. The objective of this study was to determine the role of cerebral cell-column chromatography in quantifying cell volumes of individual cerebral cell lines, under chemically-induced anoxia/re-oxygenation (A/R). Cerebral endothelial cells (4 experiments) or type II astrocytes (4 experiments) were cultured to confluence on microcarrier beads. A chromatographic cell-column of 1.5 cm height was filled with non-treated cell-covered beads. The column was perfused at 1 ml/min with a balanced perfusate for one hour (Baseline). The perfusate was then switched to that containing 5 mM thioglycolic acid for one hour (Anoxia). Then the column was perfused with the normal perfusate for another two hours (Re-oxygenation). The total free space in the column, reversely reflecting cell volumes, was determined by averaged transit time (TTa) of a non-permeable flow tracer blue dextran. Decreased TTa means that cells swell, and vice versa. TTa in endothelial cell columns increased with a peak at 60 minutes of re-oxygenation. TTa in astrocyte columns decreased with a nadir at 30 minutes of re-oxygenation. Cell column chromatography can be used to determine the cerebral cell volume changes following chemically-induced anoxia/re-oxygenation.
    Acta neurochirurgica. Supplement 02/2005; 95:411-4.
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    ABSTRACT: Ifenprodil, a NMDA receptor polyamine site antagonist, reduces experimental cardiac arrest (CA)-elicited brain edema, which is associated with an up-regulation of aquaporin 4 (AQP4), a brain water-selective channel. However, the interacting roles of NMDA receptors and AQP4 in CA-elicited brain edema are unknown. The objective of this study was to test our hypothesis that ifenprodil treatment is associated with a down-regulation of brain AQP4. Twenty-five rats were assigned to normal controls (group 1, n = 6) or subjected to eight minutes of asphyxial CA treated with placebo (group 2, n = 9) or ifenprodil (group 3, n = 10). Ifenprodil at 10 mg/kg or normal saline of equal volume was given intraperitoneally, 5 minutes before CA. The density of AQP4 protein and actin bands was scanned and expressed as the ratios of the optical density of AQP4 relative to that of actin. The ANOVA analysis was used to compare the group differences. The ratios of the optical density of AQP4 to that of actin were 0.88 +/- 0.06 in group 1, 1.11 +/- 0.08 in group 2 (p < 0.05 vs. group 1), and 0.78 +/- 0.04 in group 3 (p < 0.01 vs. group 2; NS vs. group 1). Ifenprodil given before CA is associated with a downregulation of brain AQP4 in rats.
    Acta neurochirurgica. Supplement 01/2005; 95:415-9.
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    ABSTRACT: The antiatherogenic properties of apoA-IV suggest that this protein may act as an anti-inflammatory agent. We examined this possibility in a mouse model of acute colitis. Mice consumed 3% dextran sulfate sodium (DSS) in their drinking water for 7 days, with or without daily intraperitoneal injections of recombinant human apoA-IV. apoA-IV significantly and specifically delayed the onset, and reduced the severity and extent of, DSS-induced inflammation, as assessed by clinical disease activity score, macroscopic appearance and histology of the colon, and tissue myeloperoxidase activity. Intravital fluorescence microscopy of colonic microvasculature revealed that apoA-IV significantly inhibited DSS-induced leukocyte and platelet adhesive interactions. Furthermore, apoA-IV dramatically reduced the upregulation of P-selectin on colonic endothelium during DSS-colitis. apoA-IV knockout mice exhibited a significantly greater inflammatory response to DSS than did their WT littermates; this greater susceptibility to DSS-induced inflammation was reversed upon exogenous administration of apoA-IV to knockout mice. These results provide the first direct support for the hypothesis that apoA-IV is an endogenous anti-inflammatory protein. This anti-inflammatory effect likely involves the inhibition of P-selectin-mediated leukocyte and platelet adhesive interactions.
    Journal of Clinical Investigation 08/2004; 114(2):260-9. · 12.81 Impact Factor
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    ABSTRACT: Brain edema occurs in experimental and clinical cardiac arrest (CA) and is predictive of a poor neurological outcome. N-Methyl--aspartate (NMDA) receptors contribute to brain edema elicited by focal cerebral ischemia/reperfusion (I/R). Ifenprodil, a NMDA receptor antagonist, attenuates brain edema and injury size in rats after focal cerebral I/R. We assessed the hypothesis that ifenprodil reduces CA-elicited brain edema. Eighteen male Sprague-Dawley rats were assigned to group 1 (normal control, n=6), group 2 (placebo-treated CA, n=6), or group 3 (ifenprodil-treated CA, n=6). CA was induced by 8 min of asphyxiation and the animals were resuscitated with cardiopulmonary resuscitation (CPR), ventilation, epinephrine (adrenaline), and sodium bicarbonate (NaHCO3). Ifenprodil of 10 mg/kg or a placebo vehicle was given intraperitoneally 5 min before CA. Brain edema was determined by brain wet-to-dry weight ratio at 1 h after resuscitation. There were no differences between groups 2 and 3 in all physiological variables at baseline. Time from asphyxiation to CA was 201.5 +/- 7.5 s in group 2 and 160.7 +/- 10.4 s in group 3 (P<0.001). Resuscitation time was 68.2 +/- 13.3 s in group 2 and 92.8 +/- 18.2 s in group 3 (P<0.05). Ifenprodil decreased mean arterial pressure (MAP) before asphyxiation, from 128 +/- 7 in group 2 to 82 +/- 15 mmHg in group 3 (P<0.001), and negated immediate post-resuscitation hypertension. Brain wet-to-dry weight ratio was 5.64 +/- 0.44 in group 1, 7.34 +/- 0.95 in group 2 (P<0.01 versus group 1), and 5.93 +/- 0.40 in group 3 (P<0.05 versus group 2). Ifenprodil reduces CA-elicited brain edema. In addition, we observed significant hemodynamic changes caused by ifenprodil.
    Resuscitation 06/2004; 61(2):209-19. · 4.10 Impact Factor
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    ABSTRACT: Previous studies indicate that deficiency of endothelial nitric oxide (NO) synthase (eNOS)-derived NO exacerbates myocardial reperfusion injury. We hypothesized that overexpression of eNOS would reduce the extent of myocardial ischemia-reperfusion (MI/R) injury. We investigated two distinct strains of transgenic (TG) mice overexpressing the eNOS gene (eNOS TG). Bovine eNOS was overexpressed in one strain (eNOS TG-Kobe), whereas the human eNOS gene was overexpressed in the other strain (eNOS TG-RT). Non-TG (NTG) and eNOS TG mice were subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion, and the extent of myocardial infarction was determined. Myocardial infarct size was reduced by 33% in the eNOS TG-Kobe strain (P < 0.05 vs. NTG) and by 32% in the eNOS TG-RT strain (P < 0.05 vs. NTG). However, postischemic cardiac function (cardiac output, fractional shortening) was not improved in the eNOS TG-Kobe mouse at 24 h of reperfusion [P = not significant (NS) vs. NTG]. In additional studies, eNOS TG-Kobe mice were subjected to 30 min of myocardial infarction and 7 days of reperfusion. Fractional shortening and the first derivative of left ventricular pressure were measured in eNOS TG-Kobe and NTG mice, and no significant differences in contractility were observed (P = NS) between the eNOS TG mice and NTG controls. Left ventricular end-diastolic pressure was significantly (P < 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion. The cardioprotective effects of eNOS overexpression on myocardial infarct size were ablated by Nomega-nitro-l-arginine methyl ester (300 mg/kg) pretreatment. Thus genetic overexpression of eNOS in mice attenuates myocardial infarction after MI/R but fails to significantly protect against postischemic myocardial contractile dysfunction in mice.
    AJP Heart and Circulatory Physiology 02/2004; 286(1):H276-82. · 4.01 Impact Factor
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    ABSTRACT: Reduced plasma concentrations of the extracellular actin-binding proteins gelsolin and Gc-globulin correlate with pulmonary failure and death in humans after injury. The purpose of this study was to investigate the role of plasma gelsolin in the pathophysiology of inflammation-induced lung injury. We postulated that plasma gelsolin levels decrease at an early time point after burn injury and that the intravenous infusion of gelsolin prevents burn-induced pulmonary microvascular dysfunction. Adult Sprague-Dawley rats were randomized to undergo a 40% body surface area thermal injury (Burn) or manipulation without burn (Sham). Plasma gelsolin and Gc-globulin concentrations were determined at various times during the first 6 days of injury by Western blotting. Other animals were randomized to receive either recombinant human gelsolin (0.078, 0.78, or 7.8 mg) or albumin (7.8 mg) before and 8 h after Burn or Sham. Twenty-four hours later, pulmonary microvascular permeability was assessed by measuring the capillary filtration by use of an isolated, perfused lung model. We found that plasma gelsolin levels of burn-injured rats decreased to 10% of normal levels within 12 h and remained below normal levels for up to 6 days postinjury. Gc-globulin values also fall, but to a lesser extent and only transiently. Treatment of burned animals with intravenous infusions of recombinant human gelsolin prevented the increase in pulmonary microvascular permeability that accompanies this injury. Our findings are consistent with the hypothesis that plasma gelsolin depletion contributes to the pathophysiology of pulmonary microvascular dysfunction during inflammation.
    Journal of Applied Physiology 02/2004; 96(1):25-31. · 3.48 Impact Factor
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    ABSTRACT: Arteriovenous carbon dioxide (AVCO2R) removal is a technique of pumpless extracorporeal carbon dioxide removal. This system has been used successively to control pH and PaCO2 in patients with acute lung injury who could not be adequately ventilated. This report describes the use of this technology in an organ donor awaiting harvesting. AVCO2R was implanted using a hollow-fiber oxygenator attached to 12 F and 14 F vascular cannulas that were inserted into the femoral artery and vein, respectively. Oxygen was attached to the oxygenator to provide the sweep gas. The PaCO2 and arterial pH promptly corrected after support was initiated (from 83-42 mm Hg and 7.18-7.38, respectively). This case describes the successful use of pumpless arteriovenous extracorporeal removal of CO2 in a heart-beating donor awaiting organ harvest.
    Transplantation 01/2004; 76(11):1630-2. · 3.78 Impact Factor
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    ABSTRACT: Liver ischaemia-reperfusion (I/R) occurs during resuscitation from haemorrhagic shock, hepatic transplantation and anatomic resection of the liver. This injury is associated with hepatocellular enzyme release and hepatocyte necrosis. The impact of chronic illnesses such as diabetes mellitus (DM) on hepatic I/R is unknown. This study determines the effect of DM on liver I/R using a murine model of type II DM in which the leptin receptor is defective. Preliminary studies suggest that animal models of DM have impaired endothelial nitric oxide (NO) release. Other studies suggest that NO attenuates hepatic I/R in phenotypically normal animals. We postulated that DM exacerbates hepatic I/R and that exogenous NO administration will attenuate hepatocellular injury. Non-diabetic and diabetic (db/db) mice were anaesthetized and underwent laparotomy with the placement of a microvascular clip on the hepatic artery and portal vein supplying the medial and left lateral lobes of the liver rendering about 70% of the liver ischaemic. Hepatic ischaemia was maintained for 45 min after which time the clip was removed and the liver segments reperfused. The abdomen was closed and the animals maintained for 5 h of reperfusion. Hepatic injury was then assessed by measuring serum alanine and aspartate transaminases (ALT, AST) spectrophotometrically. Sections of liver reperfused for 24 h were stained with haematoxylin and eosin and the percentage of hepatocyte necrosis evaluated using morphometric techniques. Other animals undergoing hepatic I/R received the NO donor (DETA 100 micro g/kg, i.v. 5 min prior to reperfusion). Time-matched, sham-operated animals served as controls. The data are expressed as mean +/- SEM and analysed by ANOVA. Serum AST and ALT levels were significantly higher in db/db animals vs. non-diabetics, even in the absence of hepatic I/R (P < 0.01). Serum AST and ALT levels in db/db mice undergoing hepatic I/R were nearly five times greater than that of non-diabetic animals (P < 0.01). Histologic examination of the livers of the diabetic animals undergoing I/R demonstrated significantly greater hepatocellular necrosis (zone III; 30-40%) when compared with non-diabetic animals sustaining the same injury (zone III; 3-10%). The NO donor DETA totally prevented the increase in serum ALT and AST release associated with I/R in both the diabetic and non-diabetic mice when compared with animals not receiving this agent (P < 0.01). This is the first study suggesting that DM exacerbates hepatic I/R and that NO donors will prevent this hepatocellular injury in the diabetic. Sixteen million Americans have DM. Understanding the effect of this chronic illness on the inflammatory response to injury is essential to improving clinical outcomes in these medically compromised patients.
    Clinical Transplantation 01/2004; 18 Suppl 12:7-11. · 1.63 Impact Factor
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    ABSTRACT: Without Abstract
    Annals of Surgical Oncology 01/2004; 11. · 4.12 Impact Factor

Publication Stats

1k Citations
218.32 Total Impact Points

Institutions

  • 2002–2009
    • Louisiana State University Health Sciences Center New Orleans
      • Department of Surgery
      Baton Rouge, LA, United States
  • 2002–2006
    • Louisiana State University Health Sciences Center Shreveport
      Shreveport, Louisiana, United States
  • 2004
    • Louisiana State University in Shreveport
      Shreveport, Louisiana, United States
    • University of Texas Medical School
      • Department of Surgery
      Houston, Texas, United States
  • 1994–2003
    • University of Texas Southwestern Medical Center
      • Department of Surgery
      Dallas, TX, United States
  • 2000
    • University of Texas at Dallas
      Richardson, Texas, United States
  • 1997
    • Temple University
      • Department of Surgery
      Philadelphia, PA, United States
  • 1989–1992
    • Concordia University‚ÄďAnn Arbor
      Ann Arbor, Michigan, United States