The Journal of surgical research最新文献

{"title":"Left ventricular end-diastolic volume from ejection fraction and stroke volume in pigs during IVC occlusion.","authors":"Cecily J. Gallup, S. E. Cabreriza, J. Hart, R. Walsh, A. Weinberg, H. M. Spotnitz","doi":"10.1006/JSRE.2002.6432","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6432","url":null,"abstract":"BACKGROUND\u0000Real-time measurement of left ventricular end-diastolic volume (LVEDV), combined with left ventricular end-diastolic pressure (LVEDP), would allow continuous measurement of intraoperative diastolic function. In pursuit of this goal, we examined stroke volume divided by ejection fraction for calculation of LVEDV(sv/ef).\u0000\u0000\u0000METHODS\u0000Five anesthetized pigs underwent median sternotomy and pericardiotomy. A transit-time ultrasonic flow probe on the ascending aorta provided cardiac output. A micromanometer provided LV end-diastolic pressure. End-diastolic and end-systolic areas were measured from LV short-axis cross sections to obtain ejection fraction. LVEDV(sv/ef) was calculated during IVC occlusion. Steady-state LVEDV(echo) was determined using a three-plane echocardiography model. LVEDV(echo) was used to validate steady-state LVEDA in each experiment.\u0000\u0000\u0000RESULTS\u0000Correlation coefficients for linear and pressure-volume relation analyses ranged from 0.46 to 0.99. The two methods for measuring LVEDV generated compliance curves with an overall reliability coefficient of 0.84.\u0000\u0000\u0000CONCLUSIONS\u0000The LVEDV(sv/ef) method may facilitate real-time determination of LV compliance.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"538 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124525487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitric oxide inhibition increases aortic wall matrix metalloproteinase-9 expression.","authors":"M. Eagleton, D. A. Peterson, V. Sullivan, K. Roelofs, J. A. Ford, J. Stanley, G. Upchurch","doi":"10.1006/JSRE.2002.6396","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6396","url":null,"abstract":"OBJECTIVE\u0000Nitric oxide (NO) may mediate vessel wall remodeling by regulating expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). This study tested the hypothesis that nitric oxide synthase (NOS) inhibition in whole aortic wall causes increases in cytokine-stimulated MMP and TIMP expression.\u0000\u0000\u0000METHODS\u0000Cultured infrarenal aortic segments from Sprague-Dawley rats were exposed to increasing concentrations (0, 0.1, 0.5, 1, and 5 mM; n = 6 per concentration) of N(G)-monomethyl-l-arginine (L-NMMA), a known inhibitor of NOS. This was in the presence of 2 ng/ml of interleukin-1beta, a known inducer of NOS, MMP, and TIMP expression. Media nitrate and nitrite (NO(x)) were measured at 72 h using the Saville method. Media MMP activity was measured using gelatin zymography. MMP-2 and -9 protein and mRNA levels were determined by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). TIMP activity and mRNA levels were evaluated by reverse zymography and RT-PCR. Data were analyzed using ANOVA.\u0000\u0000\u0000RESULTS\u0000Increasing concentrations of L-NMMA produced a dose-dependent decrease in NO(x) (2214 +/- 405 to 347 +/- 37 ng/mg, P < 0.001). Zymography demonstrated a dose-dependent increase in 92-kDa MMP (pro-MMP-9) activity (P < 0.001) with corresponding increases in pro-MMP-9 protein (P = 0.03) and mRNA levels (P = 0.004). While there was a dose-dependent increase in 72-kDa MMP (pro-MMP-2) activity (P = 0.001), pro-MMP-2 protein and mRNA levels were unchanged. Reverse zymography demonstrated a dose-dependent increase in 29-kDa TIMP-1 activity (P = 0.01), but there was no change in TIMP-1 mRNA levels.\u0000\u0000\u0000CONCLUSIONS\u0000NOS inhibition in ex vivo aortic tissue causes a dose-dependent increase in MMP-9 expression and activity. It is speculated that deficiencies of NO in vivo alter MMP and TIMP homeostasis, favoring matrix degradation.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115039000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Military trauma training performed in a civilian trauma center.","authors":"M. Schreiber, J. Holcomb, C. Conaway, Kyle D. Campbell, M. Wall, K. Mattox","doi":"10.1006/JSRE.2002.6391","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6391","url":null,"abstract":"BACKGROUND\u0000In 1996, Congress passed legislation requiring the Department of Defense to conduct trauma training in civilian hospitals. In September of 1998 an Army team composed of surgeons, nurses, emergency medical technicians (EMTs), and operating room technicians (OR techs) trained in a civilian level 1 trauma center. This study analyzes the quality of the training.\u0000\u0000\u0000METHODS\u0000The training period was 30 days. Before and after training all members completed a questionnaire of their individual and team ability to perform at their home station, at the civilian hospital, and in the combat setting. Surgeons maintained an operative log, which was compared with their prior year's experience. Primary trauma cases (PTCs) met Residency Review Committee criteria as defined category cases and were done acutely. Other personnel tracked the percentage of supporting soldier tasks (SSTs) they performed or were exposed to during the training period.\u0000\u0000\u0000RESULTS\u0000Review of the questionnaires revealed a significant increase in confidence levels in all areas tested (P < 0.005). The three general surgeons performed a total of 42 PTCs during the 28 call periods, or 1.5 PTCs per call period. During the prior year, the same three general surgeons performed 20 PTCs during 114 call periods for 0.175 cases per call period (P = 0.003). The maximum number of PTCs performed during one call period at the civilian center was 4, compared with 5 PTCs performed by one Army surgeon during the Somalia 1993 mass casualty event. Performance of or exposure to SSTs was 71% for the EMTs, 94% for the nurses, and 79% for the OR techs.\u0000\u0000\u0000CONCLUSIONS\u0000A 1-month training experience at a civilian trauma center provided military general surgeons with a greater trauma experience than they receive in 1 year at their home station. Other personnel on the team benefited by performing or being exposed to their SSTs. Further training of military teams in civilian trauma centers should be investigated.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"67 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124993337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association for Academic Surgery, an idea whose time has come?","authors":"D. Berger","doi":"10.1006/JSRE.2002.6375","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6375","url":null,"abstract":"I thank Dr. Ko for his kind introduction. Membership in the Association for Academic Surgery has been a highlight of my professional career. I have attempted to contribute as much to the organization as the organization has contributed to my professional growth. It has been an honor and a privilege to serve as a member of the Committee on Issues, the chair of the Committee on Issues, the secretary, the president elect, and this past year as the 34th president of the association. The most rewarding aspect of my time in the AAS has been the many friendships and collaborations I have developed. The AAS has afforded me the opportunity to get to know and interact with some of the most talented young surgeons in the world. For that opportunity I am grateful. The past year has been an exciting one. It has been a true joy working with the officers, the council members, and the staff of our management firm. The most difficult aspect of being AAS president has been the preparation for this moment. I have pondered my message for 2 years, hoping for divine inspiration. Two years ago, Past President Souba, as Dr. Klimberg’s invited speaker, discussed the need for academic leadership and the role of the AAS. He challenged the AAS membership to develop programs concerning leadership and leadership training [1]. I was inspired and determined to make leadership the focus of the 35th Annual Meeting of the AAS and of my address. I was going to discuss the practical aspects of a midcareer move to a leadership position. Hence, the title “From Led to Leader,” published in the announcements. However, the events of September 11 have had a profound impact on all our lives and our view of the world. I am certain there are few, if any, in this room who did not lose a loved one or know someone who lost","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"12 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128016072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular smooth muscle cells derived from atherosclerotic human arteries exhibit greater adhesion, migration, and proliferation than venous cells.","authors":"P. Faries, D. Rohan, M. Wyers, M. Marin, L. Hollier, W. Quist, F. Logerfo","doi":"10.1006/JSRE.2002.6399","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6399","url":null,"abstract":"BACKGROUND\u0000Phenotypic variation of vascular smooth muscle cells (VSMC) may result in altered biological behavior and responses. Within the vessel wall, arterial VSMC have a greater propensity to form atherosclerotic lesions as compared to venous VSMC. In this study the rates of proliferation, adhesion, and migration were compared between VSMC of atherosclerotic arterial and venous origin.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Human VSMC cultures were isolated from 18 infragenicular arteries at the time of below knee amputation and from 20 saphenous veins during lower extremity revascularization surgery. Cell cultures were isolated from the media of each specimen and maintained in distinct cell lines for all assays. Cells from passages 2 and 3 were assayed for their proliferative capacity using total DNA fluorescence photometry and for adhesion and migration using a modified Boyden chamber.\u0000\u0000\u0000RESULTS\u0000Patient age and the incidence of atherosclerotic risk factors did not vary significantly between the arterial and the venous patient groups. VSMC of atherosclerotic arterial origin demonstrated greater proliferation (arterial, 162 +/- 59 absorption units, vs. venous, 106 +/- 56 absorption units, P < 0.001), adhesion (arterial, 74.1 +/- 22.6 cells/microscopic field, vs. venous, 41.3 +/- 12.8 cells/microscopic field, P < 0.001) and migration (arterial, 427 +/- 185 cells/microscopic field, vs venous, 119 +/- 101 cells/microscopic field, P < 0.001) than VSMC of venous origin.\u0000\u0000\u0000CONCLUSION\u0000Human atherosclerotic arterial VSMC exhibit significantly increased rates of proliferation, adhesion, and migration as compared to human venous VSMC. These observations of VSMC in culture are consistent with the clinical predilection for the hyperplasic responses that result in the development of atherosclerosis in the arterial wall. Possible intrinsic differences in VSMC phenotype should be considered in designing methods to limit atherosclerosis.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"65 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124321352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular effects of poly-N-acetylglucosamine in isolated rat aortic rings.","authors":"Y. Ikeda, L. Young, J. Vournakis, A. M. Lefer","doi":"10.1006/JSRE.2001.6323","DOIUrl":"https://doi.org/10.1006/JSRE.2001.6323","url":null,"abstract":"BACKGROUND\u0000[corrected] Poly-N-acetylglucosamine (p-GlcNAc) is a secretion of marine diatoms that is known to be useful in controlling bleeding. As a component of promoting hemostasis, p-GlcNAc is thought to exert vasoconstrictor effects in arteries. The present study was undertaken to determine whether p-GlcNAc induced a significant vasoconstrictor effect and, if so, what the mechanism of this effect might be.\u0000\u0000\u0000MATERIALS AND METHODS\u0000We examined vascular effects of p-GlcNAc on isolated aortic rings obtained from Sprague-Dawley rats. The rings were suspended in organ baths and precontracted with U46619, a thromboxane A2 mimetic.\u0000\u0000\u0000RESULTS\u0000p-GlcNAc produced a concentration-dependent vasoconstriction over the range of 14 to 100 microg/ml. At a concentration of 100 microg/ml, p-GlcNAc significantly contracted aortic rings by 133 +/- 20 mg of developed force (P < 0.01). Neither a deacetylated derivative of p-GlcNAc nor a structurally related macromolecule, chitin, contracted rat aortic rings, indicating a specificity for p-GlcNAc. The vasoconstriction to p-GlcNAc was totally abolished in deendothelialized rat aortic rings, suggesting that an endothelial component is essential to the vasoconstriction. Pretreatment with the endothelin ET(A) receptor antagonist, JKC-301 (0.5 and 1 microM), significantly diminished p-GlcNAc-induced vasoconstriction by 57 to 61% (P < 0.01). However, p-GlcNAc did not significantly diminish nitric oxide release from rat aortic endothelium.\u0000\u0000\u0000CONCLUSION\u0000These results provide evidence that p-GlcNAc significantly contracts isolated rat aortic rings via an endothelium-dependent mechanism, partly via enhancement of endothelin-1 release from endothelial cells.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"159 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"119596477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-color flow cytometric study on lymphocytes derived from thymic diseases.","authors":"M. Okumura, Y. Fujii, S. Miyoshi, H. Shiono, M. Inoue, Y. Kadota, K. Fukuhara, H. Matsuda","doi":"10.1006/JSRE.2001.6282","DOIUrl":"https://doi.org/10.1006/JSRE.2001.6282","url":null,"abstract":"BACKGROUND\u0000Anterior mediastinal masses derive from a variety of diseases. Thymomas have been shown to commonly hold CD4(+)CD8(+) double-positive (DP) lymphocytes, and identification of this subset by two-color flow cytometric study was suggested to help diagnosis of thymoma. Several other thymic diseases, however, possibly hold CD4(+)CD8(+) DP lymphocytes. In this study, we utilized the three-color flow cytometric method for further examination of the phenotypes of lymphocytes in the thymic diseases.\u0000\u0000\u0000MATERIALS AND METHODS\u0000One hundred eight specimens (77 primary and 10 metastatic thymomas, 10 thymic carcinomas, 2 thymic carcinoids, 4 malignant lymphomas, 2 seminomas, an inflammatory pseudotumor, and 2 nonneoplastic thymic hyperplasias) were subjected to the study. The expressions of CD3, CD4, and CD8 on tumor-associated lymphocytes were evaluated by three-color flow cytometric study.\u0000\u0000\u0000RESULTS\u0000The proportion of the CD4(+)CD8(+) DP subset was more than 30% in all 78 lymphocyte-rich thymomas, in 2 malignant lymphomas, and in both thymic hyperplasias. CD3 expression of the CD4(+)CD8(+) DP subset ranged from a negative to a high level in thymomas and thymic hyperplasias, while it was restricted to a particular level in CD4(+)CD8(+) DP-type malignant lymphomas. The proportion of CD3(+) cells in the CD4(+)CD8(-) single-positive subset was consistently less than 90% in the lymphocyte-rich thymomas, while it was more than 90% in the thymic hyperplasias.\u0000\u0000\u0000CONCLUSION\u0000Although identification of the CD4(+)CD8(+) DP subset in the tumor-associated lymphocytes does not necessarily indicate thymoma, a further characterization of thymic neoplasms possessing the CD4(+)CD8(+) DP subset was enabled by three-color flow cytometric study, suggesting the utility of this method as an ancillary tool for differential diagnosis of these diseases.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"390 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"118742921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pravastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, attenuates renal injury in an experimental model of ischemia-reperfusion.","authors":"M. Joyce, C. Kelly, D. Winter, G. Chen, A. Leahy, D. Bouchier‐Hayes","doi":"10.1006/JSRE.2001.6256","DOIUrl":"https://doi.org/10.1006/JSRE.2001.6256","url":null,"abstract":"BACKGROUND\u0000Renal dysfunction due to ischemia-reperfusion (IR) injury is a common problem following renovascular surgery or kidney transplantation. There is a lot of emerging evidence that statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, have anti-inflammatory properties and exert direct beneficial effects on the vascular endothelium. The aim of this study was to determine if pretreatment with pravastatin would attenuate the acute renal dysfunction that occurs following IR injury in an experimental model.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Male Sprague-Dawley rats were randomized into four groups (n = 7 per group): control, uninephrectomy, IR group, and IR group pretreated with pravastatin (0.4 mg/kg/day for the preceding 5 days). Following a left nephrectomy the IR injury was induced by cross-clamping the right vascular pedicle for 30 min followed by reperfusion for 2 h. In a separate experiment (n = 6 per group) renal function was assessed 12 and 24 h after reperfusion.\u0000\u0000\u0000RESULTS\u0000IR injury causes significant renal dysfunction characterized by oliguria, 0.11 (0.05) ml/h, decreased glomerular filtration rate (GFR), 0.02 (0.01) ml/min; and marked protein leakage, 7.21 (1.3) g/L, 2 h postreperfusion. This renal dysfunction was also evident 12 and 24 h postreperfusion. This was in contrast to values of 0.61 (0.13) ml/h, 0.23 (0.01) ml/min, and 1.67 (0.12) g/L in the uninephrectomy-only group and values of 2 ml/h, 7.3 ml/min, and 0.72 g/L for uninjured time-matched controls. Pretreatment with pravastatin significantly attenuated IR-induced renal injury, improving urine production to 0.62 (0.2) ml/h and GFR to 0.14 (0.02) ml/min and diminishing protein leakage to 3.76 (0.7) g/L at the 2-h time point. This renoprotective effect was also evident 12 and 24 h postreperfusion. This renal protection was associated with an upregulation of constitutive endothelial nitric oxide synthase in the pravastatin-treated group.\u0000\u0000\u0000CONCLUSION\u0000These results show that pravastatin may play a role in modulating renal impairment following aortic or transplantation surgery, allowing earlier recovery from an IR injury.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120787206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytosolic phospholipase A(2)-mediated ICAM-1 expression is calcium dependent.","authors":"C. Barnett, E. Moore, C. Silliman, E. Abdalla, D. Partrick, S. Curley","doi":"10.1006/JSRE.2001.6188","DOIUrl":"https://doi.org/10.1006/JSRE.2001.6188","url":null,"abstract":"BACKGROUND\u0000Some human malignancies such as virus-related hepatocellular cancer arise in a setting of chronic inflammation. Upregulation of ICAM-1 is a seminal late event in malignant transformation following chronic inflammation. Cytosolic phospholipase A(2) (cPLA(2)) is a lipid-mediator activated by inflammatory stimuli, which has been shown to mediate ICAM-1 upregulation. As lipid mediators are known to work via calcium-dependent mechanisms in nearly all mammalian cells, we hypothesize that inflammatory-mediated ICAM-1 upregulation is dependent on both cPLA(2) and intracellular calcium.\u0000\u0000\u0000MATERIALS AND METHODS\u0000HUVEC were chosen as a representative cell line as they emulate hepatic sinusoids and are a well-established cell model. These were grown to confluence in T-25 flasks and stimulated with TNF-alpha or LPS for 6 h. Additional groups were preincubated with AACOCF3 (a specific cPLA(2) inhibitor) or BAPTA A.M. (a specific inhibitor of intracellular Ca(2+)) prior to being exposed to inflammatory stimuli. ICAM-1 expression was determined by mean fluorescent intensity (MFI) as measured by FITC-labeled moAb to ICAM-1 via FACS. The role of intracellular Ca(2+) on cPLA(2) activity was determined by thin-layer chromatography. Groups were compared using ANOVA with Scheffe's post hoc analysis; *P < 0.05 vs control, daggerP < 0.05 vs LPS and TNF-alpha was considered significant; N > or = 4 all experimental groups.\u0000\u0000\u0000RESULTS\u0000Both cPLA(2) and Ca(2+) inhibition significantly inhibited inflammatory upregulation of ICAM-1. Pretreatment with BAPTA A.M. attenuated HUVEC cPLA(2) activity in response to LPS. These findings suggest that appropriate molecular target suppression may prevent malignant degeneration in the presence of chronic inflammation.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"57 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127492639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of ischemia on gene expression.","authors":"J. Huang, R. Qi, John Quackenbush, E. Dauway, E. Lazaridis, T. Yeatman","doi":"10.1006/JSRE.2001.6195","DOIUrl":"https://doi.org/10.1006/JSRE.2001.6195","url":null,"abstract":"Microarray gene expression technology has recently made it feasible to characterize the RNA expression of thousands of genes across numerous tissue samples. We hypothesized that the warm ischemia commonly associated with the surgical extirpation of human tissue would have significant effects on gene expression profiles. To quantitate the effects of warm ischemia on human tissue, we rapidly dissected normal mucosa from a human colon cancer specimen. The specimen was divided and maintained at room temperature until snap-frozen in liquid nitrogen. Aliquots of tissue were frozen at times 5, 10, 15, 20, 40, and 60 min after extirpation. Spotted microarrays composed of 2400 distinct elements were used to assay mRNA derived from each time point in triplicate. Eisen's hierarchical clustering methodology and Bayesean statistical methods were then used to assay the effects of warm ischemia on gene expression. Application of time-course statistical models suggest that three patterns were induced by ischemia, accounting for 68.2, 17.8, and 13.4% of the evaluable genes, respectively. Pattern I corresponds to an average change of 27% over 60 min from 5 min baseline level of expression and 63.8% of the genes with at least 80% probability of membership in this pattern show average increases in expression over 60 min. The remainder decrease on average. Pattern II genes show the least ischemia-related effects, demonstrating an average change of only 12% over 60 min. In contrast to pattern I, we find that 67.5% of the genes with at least 80% probability of membership in this pattern are decreasing in expression on average over time. The remaining 32.5% in this pattern increase an average of 12% over 60 min. Finally, pattern III genes (13.4% of the sample) show the greatest sensitivity to ischemia, changing an average of 50% over 60 min, with about the same number increasing as are decreasing. Fold changes in RNA over- or under-expression were observed up to greater than 20-fold. Warm ischemia associated with the surgical extirpation of human tissues has significant effects on gene expression. These data support the careful monitoring of ischemic time for tissues harvested for the purpose of gene profiling.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"107 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127326387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}