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Biomedical subjects

Rebecca M Minter

Publications and source records attributed to Rebecca M Minter.

13 recordsLinked to original sources
PubMed2006

Construct validity of the LapSim laparoscopic surgical simulator.

BACKGROUND: Computer-aided simulators may increase the safety and efficiency of training in laparoscopic surgery. Before implementation of the Immersion LapSim (Gaithersburg, MD) simulator in our training curriculum, we wished to determine its construct validity (ie, whether the simulator could differentiate laparoscopic novices from trainees with greater experience). METHODS: Subjects were medical students (MS), residents (RES), and laparoscopic faculty (FAC). Subjects performed 10 repetitions of 6 LapSim tasks. The LapSim measured performance in 6 to 10 parameters per task, and performance was compared between groups. Post hoc t tests were used to make pair-wise comparisons among the 3 groups using the Bonferroni technique. Statistical significance was set at P < .05. RESULTS: The degree of prior laparoscopic experience was reflected in performance on at least 1 parameter for each task. Several patterns of performance between MS, RES, and FAC were observed. CONCLUSIONS: The LapSim has performance parameters that reliably differentiate between subjects with varying laparoscopic experience. However, some performance parameters do not differentiate between groups. To accurately measure a trainee's skill level, only parameters that sensitively measure the true level of performance should be used.

Computer Simulation↗
PubMed2006

Laparoscopic skills are improved with LapMentor training: results of a randomized, double-blinded study.

OBJECTIVE: To determine if prior training on the LapMentor laparoscopic simulator leads to improved performance of basic laparoscopic skills in the animate operating room environment. SUMMARY BACKGROUND DATA: Numerous influences have led to the development of computer-aided laparoscopic simulators: a need for greater efficiency in training, the unique and complex nature of laparoscopic surgery, and the increasing demand that surgeons demonstrate competence before proceeding to the operating room. The LapMentor simulator is expensive, however, and its use must be validated and justified prior to implementation into surgical training programs. METHODS: Nineteen surgical interns were randomized to training on the LapMentor laparoscopic simulator (n = 10) or to a control group (no simulator training, n = 9). Subjects randomized to the LapMentor trained to expert criterion levels 2 consecutive times on 6 designated basic skills modules. All subjects then completed a series of laparoscopic exercises in a live porcine model, and performance was assessed independently by 2 blinded reviewers. Time, accuracy rates, and global assessments of performance were recorded with an interrater reliability between reviewers of 0.99. RESULTS: LapMentor trained interns completed the 30 degrees camera navigation exercise in significantly less time than control interns (166 +/- 52 vs. 220 +/- 39 seconds, P < 0.05); they also achieved higher accuracy rates in identifying the required objects with the laparoscope (96% +/- 8% vs. 82% +/- 15%, P < 0.05). Similarly, on the two-handed object transfer exercise, task completion time for LapMentor trained versus control interns was 130 +/- 23 versus 184 +/- 43 seconds (P < 0.01) with an accuracy rate of 98% +/- 5% versus 80% +/- 13% (P < 0.001). Additionally, LapMentor trained interns outperformed control subjects with regard to camera navigation skills, efficiency of motion, optimal instrument handling, perceptual ability, and performance of safe electrocautery. CONCLUSIONS: This study demonstrates that prior training on the LapMentor laparoscopic simulator leads to improved resident performance of basic skills in the animate operating room environment. This work marks the first prospective, randomized evaluation of the LapMentor simulator, and provides evidence that LapMentor training may lead to improved operating room performance.

Clinical Competence↗
PubMed2006

Gene therapy with lipopolysaccharide binding protein for gram-negative pneumonia: respiratory physiology.

BACKGROUND: Lipopolysaccharide binding protein (LBP) plays an essential role in the pulmonary immune response to gram-negative bacterial infection. LBP knockout mice with gram-negative pneumonia have increased mortality compared with wild-type controls. This mortality difference can be abolished with systemic LBP gene therapy. We postulate that LBP knockout mice will develop derangements in lung physiology from gram-negative pneumonia and that these changes can be reversed with systemic LBP gene therapy. METHODS: Twelve- to 16-week-old C57BL/6 wild-type mice and/or sex, age, matched LBP knockout mice were administered 1 x 10(3) colony-forming units/mouse of Klebsiella pneumoniae by intratracheal inoculation. Treated mice were administered 5 x 10(9) plaque-forming units of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by intravenous injection 2 days before bacterial inoculation. Respiratory physiology parameters were measured preinoculation and 24 hours postbacterial inoculation. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved 7-day survival from Klebsiella pneumonia to a level equivalent to wild-type mice exposed to the same dose of bacteria (42 vs. 43% survival). LBP knockout mice given the LBP gene therapy demonstrated increased 14-day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (28 vs. 0%, p < 0.001). LBP knockout mice developed significant differences in respiratory rate, minute ventilation, and enhanced pause (Penh), when compared with wild-type mice with Klebsiella pneumonia. These respiratory derangements were prevented with adenoviral delivery of the LBP gene before K. pneumoniae inoculation. CONCLUSIONS: Gram-negative pneumonia produces measurable changes in mortality and respiratory physiology between wild-type and LBP knockout mice. These changes can be prevented in LBP knockout mice by systemic gene therapy to restore innate immunity.

Acute-Phase Proteins↗
PubMed2005

Initial use of a novel instrument to measure professionalism in surgical residents.

BACKGROUND: No universally accepted method to measure professionalism exists. We developed an instrument to measure specific aspects of professionalism in surgical residents. METHODS: Professionalism was deconstructed into 15 domains. Behavioral descriptors were determined for extreme and selected intermediate anchors. It became evident that residents could "go too far" in some professional behaviors. Therefore, although a 7-point continuous ordinal scale forms the framework, a score of 7 does not necessarily indicate the ideal. This characteristic minimizes the problem of inflated ratings. RESULTS: The instrument was utilized by attending faculty to evaluate residents and also by residents as a self-evaluation. Calculated from ordinal values, mean (SD) of the ratings across domains for faculty evaluations of residents was 4.95 (0.38) while mean for self-evaluations was 4.95 (0.39). Reliability was high (coefficient alpha 0.85). CONCLUSIONS: This instrument provides a means to measure professional behaviors during surgical residency. Repeated use will be required to thoroughly establish validity and reliability.

Accreditation↗
PubMed2005

Gender differences in the self-assessment of surgical residents.

BACKGROUND: Despite equivalent performance as assessed by objective external measures, women tend to underestimate their abilities compared with their male counterparts. METHODS: The difference in ordinal values from faculty and resident self-evaluations was calculated for each general and plastic surgery resident. Objective external performance measures were compared for female and male residents. RESULTS: Male and female residents performed equivalently. All residents underestimated their abilities compared with faculty assessment; however, general surgery residents did so to a greater degree (P < .05). Female residents demonstrated a greater degree of underestimation than did their male colleagues; however, this was not statistically significant. CONCLUSIONS: Although female resident surgeons are generally confident in their abilities, this may be in contrast to the self-perception of many female medical students. Consideration of gender differences in self-perception may be important when providing feedback to female students and residents.

Clinical Competence↗
PubMed2005

Altered Kupffer cell function in biliary obstruction.

BACKGROUND: An altered Kupffer cell (KC) response is thought to be responsible for the characteristic phenotype observed after biliary obstruction: a phenotype marked by a defect in the hepatic reticuloendothelial system and a hypersensitivity to endotoxin. Few studies, however, have directly examined KC function. We have sought to define the specific alterations in function and phenotype that occur in the KC after biliary obstruction. METHODS: KCs were isolated from female C57BL/6 mice 4 days after a sham or common bile duct ligation (CBDL) operation. Phagocytosis, oxidative burst potential, and intracellular bacterial killing were measured as markers of reticuloendothelial system function. The KC response to endotoxin was assessed by measuring tumor necrosis factor alpha and interleukin 6 levels in the media after stimulation with lipopolysaccharide (LPS) or with LPS plus LPS-binding protein (LBP). RESULTS: CBDL KCs demonstrated a significant increase in phagocytic ability and significantly decreased baseline oxidative stress, compared with Shams. The oxidative burst potential, however, was equivalent or higher for CBDL KCs. CBDL KCs also demonstrated increased numbers of viable intracellular bacteria after infection; however, it is unclear if this finding represents impaired intracellular bacterial killing or increased phagocytosis of bacteria. With respect to the KC response to endotoxin, CBDL KCs were found to be less sensitive to the stimulatory effects of LPS alone but were exquisitely sensitive to the effects of LBP. LBP levels were found to be significantly elevated in CBDL animals, and CBDL KCs demonstrated a dose-dependent, exaggerated tumor necrosis factor alpha and interleukin 6 response to LPS administered with LBP. CONCLUSIONS: KC function is clearly altered after biliary obstruction. Phagocytic ability is actually increased, although the ability of CBDL KCs to kill bacteria within the phagosome remains ill defined. CBDL KCs are exquisitely sensitive to the effects of LBP, and LBP levels are elevated after biliary obstruction. LBP may be responsible for the increased proinflammatory response observed after endotoxin challenge in animals with biliary obstruction.

Acute-Phase Proteins↗
PubMed2005

Improved survival in mice given systemic gene therapy in a gram negative pneumonia model.

BACKGROUND: We previously demonstrated an essential role for lipopolysaccharide binding protein (LBP) in the pulmonary immune response to Gram-negative bacterial infection. LBP knockout mice had significantly higher mortality, greater rates of bacteremia, and higher counts of viable bacteria in their lungs at sacrifice compared with wild-type controls. We postulate that systemic LBP gene therapy will reconstitute a protective innate immune response in LBP knockout mice and that overexpression of LBP in wild-type mice may offer a survival advantage. METHODS: 12-16 week old female C57BL/6 wild-type mice and age matched LBP knockout mice were given 5 x 10(9) PFU of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by tail vein injection. 72 hours later each mouse was administered 1 x 10(3) CFU of Klebsiella pneumoniae by intratracheal injection. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved survival from Klebsiella pneumonia to a level equivalent or better than wild-type mice exposed to the same dose of bacteria (36 versus 25%). Wild-type mice given the LBP gene therapy demonstrated increased 7 day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (68 versus 30%, p = 0.03). CONCLUSIONS: Systemic gene therapy with intravenous adenoviral vector transfer of LBP significantly improves survival in LBP knockout mice. Overexpression of LBP in wild-type mice improves survival from Klebsiella pneumonia. Raising levels of LBP in the setting of Gram-negative pneumonia may be of therapeutic benefit.

Acute-Phase Proteins↗
PubMed2004

Influence of recombinant adenovirus on liver injury in endotoxicosis and its modulation by IL-10 expression.

Adenovirus-based gene therapy offers a unique opportunity to target gene expression to the liver by systemic delivery. However, systemic administration of a first generation adenoviral construct elicits an inflammatory response leading to TNF-alpha-dependent liver injury. The aim of this study was to evaluate whether the systemic administration of recombinant adenovirus exacerbates a subsequent TNF-alpha-dependent liver injury induced by D-galactosamine and lipopolysaccharide. Surprisingly, low-dose adenovirus administration (10(5) particles) protects, while high-dose adenovirus (10(10) particles) is associated with an exaggerated hepatic inflammatory response from a subsequent D-galactosamine and lipopolysaccharide challenge. This exacerbation is TNF-alpha dependent, since treatment with a TNF inhibitor fully protects against the liver injury. Moreover, intravenous administration of an adenoviral construct expressing the anti-inflammatory protein interleukin-10 reduces TNF-alpha appearance and attenuates the increased hepatocyte injury. Taken together, this report demonstrates potential additive effects of TNF-alpha responses induced by adenovirus and other inflammatory signals, and suggests that the response can be mitigated by relative adenovirus particle dose or by inhibitors, such as TNF-binding protein or interleukin 10.

Adenoviridae↗
PubMed2003

Metastatic potential of dermatofibrosarcoma protuberans with fibrosarcomatous change.

Dermatofibrosarcoma protuberans (DFSP) is a relatively uncommon fibrohistiocytic tumor that is locally aggressive. DFSP is associated with frequent local recurrences but rarely metastasizes. It has been suggested that fibrosarcomatous change within a dermatofibrosarcoma protuberans (DFSP-FS) is associated with increased risk of local recurrence and distant metastases. Metastases remain rare, however, and are typically preceded by multiple local recurrences. We report a rare case of a DFSP-FS metastasis to the head of the pancreas without any preceding local recurrence.

Adult↗
PubMed2003

Role of endogenous interleukin-10 in local and distant organ injury after visceral ischemia-reperfusion.

The anti-inflammatory cytokine interleukin (IL)-10 has been detected in serum after visceral ischemia-reperfusion injury and exogenous IL-10 administration has been shown to attenuate the associated distant organ injury. This study was designed to examine the role that endogenous IL-10 production plays on both local and distant organ injury after visceral ischemia-reperfusion injury. Wild-type and IL-10(-/-)-null C57BL/6 mice were subjected to 20 min of supraceliac aortic occlusion or sham laparotomy. Serum and lung tissue cytokine levels (tumor necrosis factor alpha, IL-1beta, IL-6, KC/GRO, and IL-10) were measured after reperfusion (1, 2, and/or 4 h) using either enzyme-linked immunoassay or bioassay. Lung neutrophil infiltration and injury were quantified after reperfusion injury using myeloperoxidase concentration (2 h) and mean capillary permeability (4 h), respectively, whereas the direct liver injury was quantified with serum aspartate aminotransferase levels (1, 2, and 4 h). A subset of IL-10(-/-)-null animals was administered human recombinant IL-10 before the visceral ischemia and lung MPO was measured after reperfusion (2 h). Visceral ischemia-reperfusion in the wild-type and IL-10(-/-)-null mice was associated with in an increase in both serum (IL-1beta, KC/GRO, IL-6) and lung tissue (IL-1beta, KC/GRO) cytokine levels and resulted in lung neutrophil infiltration (myeloperoxidase), lung injury (mean capillary permeability) and liver injury (aspartate aminotransferase). The magnitude of the lung tissue cytokine response (IL-1beta, KC/GRO), neutrophil infiltration, and injury were greater in the IL-10(-/-)-null mice. Exogenous IL-10 resulted in a decrease in the lung neutrophil infiltration in the IL-10(-/-)-null mice. The endogenous IL-10 response to visceral ischemia-reperfusion attenuates the associated lung neutrophil infiltration and injury but has no effect upon either the hepatic injury or the magnitude of the systemic inflammatory response. The beneficial effects of IL-10 may be mediated by the inhibition of IL-1beta and KC/GRO through an endocrine rather than paracrine signal.

Animals↗
PubMed2002

Interleukin-10 fails to modulate low shear stress-induced neointimal hyperplasia.

INTRODUCTION: Overexpression of the anti-inflammatory cytokine interleukin-10 (IL-10) blocks atherosclerotic events in vivo, and IL-10 has been recently hailed as an "immunologic scalpel" for atherosclerosis. Alternatively, mice lacking IL-10 receiving atherogenic diets have increased occlusive lesions. It remains unclear whether such IL-10 modulation broadly applies to other forms of occlusive arterial remodeling. We hypothesized that lack of IL-10 would exacerbate, and exogenous or overexpression of IL-10 would abrogate low shear stress-induced neointimal hyperplasia (NIH). METHODS: Wild-type (WT) and IL-10-deficient (IL-10-/-) mice underwent unilateral common carotid artery (CCA) ligation. Low shear stress in the patent ligated artery results in remodeling and formation of neointima containing BrdU and SMC alpha-actin-positive cells. Additional groups of WT mice underwent CCA ligation and were treated daily with intraperitoneal saline or 1 microg of human IL-10. Chronic delivery gene therapy approaches were also utilized to define the role of IL-10 signaling. WT mice were treated adventitially with 1 x 10(10) adenovirus/green fluorescent protein (Ad/gfp) and an Ad/empty control to confirm the veracity of adventitial delivery. Then, Ad viral IL-10 (vIL-10), Ad/empty, and virus buffer alone were applied directly to the adventitia of the CAA immediately following ligation. In separate experiments, 1 x 10(10) Ad/empty or Ad/vIL-10 was injected intramuscularly. CCAs were perfusion fixed 28 days postligation, the time at which NIH is near maximum. RESULTS: IL-10-/- mice developed identical NIH areas compared to WT controls. Mice receiving IL-10 demonstrated NIH equivalent to saline controls. Mice receiving intramuscular or adventitial Ad/IL-10 developed high serum levels of IL-10 yet formed NIH areas similar to those of controls. Serum IL-10 levels were significantly higher (P = 0.04) with adventitial delivery. Mice treated adventitially with Ad/gfp showed reliable transfection of cells within the adventitia of CAA. No antibody to human IL-10 was found in the sera of intraperitoneal IL-10-treated mice, which failed to attenuate NIH. CONCLUSION: Under the conditions of this experiment, lack of IL-10 does not exacerbate low shear stress-induced NIH, nor does exogenous administration or overexpression of IL-10 attenuate it. Despite high serum levels of vIL-10 in mice treated with ad/vIL-10 adventitially, there appears to be no therapeutic effect despite the confirmed transfection of adventitial cells. Discrepancies between these findings and previous research may be related to IL-10 dosing, inflammation induced by the adenoviral vector, or disparities between the NIH models.

Adenoviridae↗
PubMed2002

Bioglass attenuates a proinflammatory response in mouse peritoneal endotoxicosis.

Bioglass is a bioactive, resorbable ceramic particle that was developed to assure binding to living tissues. Bioglass is currently employed to fill osseus defects in oral surgery, and it possesses both unique anti-inflammatory and antimicrobial properties. In an effort to determine whether Bioglass may be useful as an adjunct anti-inflammatory device in local inflammatory processes, we examined whether exposure of the peritoneal cavity to Bioglass would induce a pro- or anti-inflammatory response, and then modulate a subsequent proinflammatory response to endotoxin. Three- to fifty-milligram doses of 5 pm Bioglass were administered intraperitoneally in C57BL/6 mice. Total leukocyte, myeloperoxidase, and cytokine levels in the peritoneal wash fluid were determined. In addition, the peritoneal cavity was preexposed to Bioglass, and was then subjected to a subsequent endotoxin administration. All doses of Bioglass were found to induce a significant peritoneal IL-6 response; however, Bioglass did not induce a TNF-alpha, IL-1alpha, IL-10, or a white cell recruitment into the peritoneal lavage fluid. Pretreatment of the peritoneal cavity with Bioglass produced a transient reduction in the proinflammatory response to endotoxin. We conclude that exposure to Bioglass produces an IL-6 response without concurrent expression of TNF-alpha or IL-1alpha. Bioglass appears to transiently suppress the inflammatory response to endotoxin, possibly through the early induction of IL-6. These findings suggest that Bioglass may offer a unique approach in modifying the inflammatory response in local tissue compartments.

Animals↗