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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 16 (1992), S. 30-36 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Les médiateurs de l'inflammation jouent un rôle important dans la réponse locale et systémique des lésions par brûlures. Sont impliqués dans l'oedème réactionnel les oxydants et les métabolites de l'acide arachidonique. Les médiateurs ainsi que les cytokines libérés par les macrophages activés font petu-être partie d'une réponse inflammatoire généralisée. L'hyper métabolisme post-brûlure est provoqué et entretenu par ces mêmes médiateurs, surtout les cytokines TNF, IL-1, et IL-6. Les endotoxines circulantes provenant de la plaie ou du tube digestif peuvent être incriminées. La réponse post-brûlure septique est aussi maintenant reconnue comme étant une conséquence de l'inflammation, même en dehors de l'infection. La réaction inflammatoire cellulaire provoquée par les médiateurs résulte en une réaction exagérée à l'infection dans la période postopératoire immédiate. La définition des mécanismes spécifiques des lésions et médiateurs améliore les soins des brûlures, surtout depuis que beaucoup de médiateurs sont prêts à être utilisés en clinique. Il est essentiel que la médecin comprenne cette manipulation pharmacologique afin d'utiliser de façon optimale les progès à l'avenir.
    Abstract: Resumen Los mediadores inflamatorios juegan un papel mayor tanto en los fenómenos pertinentes a la quemadura local como en los referentes a la respuesta sistémica a la lesión térmica. Los oxidantes y los metabolitos del ácido araquidónico están involucrados en el proceso inicial del edema de la quemadura. Los mediadores, así como las citocinas liberadas por los macrófagos activados, también resultan en una reacción inflamatoria generalizada precoz. El hipermetabolismo tardío de la quemadura es iniciado y perpetuado por estos mismos mediadores, especialmente las citocinas, factor necrotizante tumoral, interleucina-1 e interleucina-6. La endotoxina circulante proveniente de la quemadura o del intestino también parece estar involucrada. La respuesta séptica también se roconoce ahora como resultante de la inflamación, sin que sea necesaro que existe infección. La activación de las células inflamatorias por los mediadores resulta en una exagerada respuesta a la infección del período postquemadura. La definición de los mecanismos específicos de la lesión y de los mediadores involucrados puede resultar en avance mayor en el tratamiento de la quemaduras, especialmente teniendo en cuenta que muchos inhibidores de mediadores ya se encuentran disponibles para uso clínico. Aparece esencial que el médico comprenda esta manipulación farmacológica para que sea capaz de utilizar en forma óptima los avances que se logren en al futuro.
    Notes: Abstract Inflammatory mediators play a major role in both the local burn wound and the systemic response to burn injury. Oxidant and arachidonic acid metabolites are involved in the initial burn edema process. The mediators as well as the cytokines released from activated macrophages also result in an early generalized inflammatory response. The later postburn hypermetabolism is initiated and perpetuated by these same mediators, especially the cytokines, tumor necrosis factor, interleukin-1, and interleukin-2. Circulating endotoxin from the wound or the gut also appears to be involved. The postburn septic response is now recognized to be the result of inflammation; infection is not necessary. Mediator induced priming of the inflammatory cells by the burn itself results in an exaggerated response to infection in the postburn period. Defining the specific mechanism of injury and mediators involved can result in a major improvement in burn care, especially since many mediator inhibitors are already available for clinical use. It is essential that the clinician understand this pharmacologic manipulation in order to be able to optimally utilize these future advances.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Positron emission tomography (PET) is an imaging method that employs radionuclide and tomography techniques. PET has high sensitivity for detecting breast cancer, both the primary tumor and axillary node metastasis. From June 1995 to November 1996 a total of 27 patients underwent breast operations based on PET results at Seoul National University Hospital. Whole-body PET images were obtained beginning 60 minutes after injection of 370 MBq (10 mCi) 18F-fluorodeoxyglucose. Regional scans were also obtained with transmission images. We compared the PET results with those from the physical examination and mammography. All cases were histologically confirmed. The diagnostic accuracy of PET was excellent for the primary tumor mass (97%) compared with that of the physical examination (78%) and mammography (67%). For axillary lymph node metastasis, PET had outstanding detection accuracy (96%) compared with the physical examination and mammography (74% and 60%, respectively). Whole-body PET scans made it possible to see all of the metastatic lesions at a glance in cases of metastatic or recurrent breast cancer. There was a probable correlation between the standard uptake value (SUV) and the number of axillary lymph node metastases, but in this study statistical significance was not proved because of the small number of cases. PET also could detect breast cancer in paraffin-augmented breasts. We concluded that PET is a highly sensitive, accurate diagnostic tool for breast cancer and that SUV, after more studies, could be used as an important prognostic factor.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7217
    Keywords: breast cancer ; heterogeneity ; lymph nodes ; ploidy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Human breast carcinoma is biologically heterogeneous, and its clinical course may vary from one which is indolent to one which rapidly progresses. Although it is the metastasis rather than the primary tumor that ultimately overwhelms the patients, studies concerning the DNA pattern have focused on the primary tumors. This study was undertaken to identify heterogeneities between primary tumors and metastases, and to evaluate the prognostic significance of the ploidy pattern and the S-phase fraction (SPF) of metastatic nodes in axillary node positive patients. Seventy-four frozen specimens of the primary and corresponding metastatic nodes from 37 patients have been analyzed by flow cytometry and the SPF calculated. The results of ploidy pattern analysis in primaries revealed 25 diploidy (67.6%) and 12 aneuploidy (32.4%), while those in metastasis showed 17 diploidy (46.0%) and 20 aneuploidy (54.0%). The aneuploidy group in metastatic nodes had the poorer histological grade (85.0% vs. 15.0%, p = 0.02), and more mean metastatic nodes (5.75 ± 2.10 vs. 3.05 ± 1.56, p = 0.018), and more frequent lymphatic vessel invasion (65.0% vs. 11.8%, p = 0.031) than its counterpart. Decreased expression of ER (70.6% vs. 25.0% p = 0.006) and increased expression of c-erbB2 (65.0% vs. 23.5%, p = 0.012) were observed in the aneuploidy of metastatic nodes. The group with higher SPF in metastatic nodes had more metastatic nodes (5.47 ± 2.31 vs. 4.00 ± 1.78, p = 0.042), and the higher incidence of lymphatic vessel invasion (57.9% vs. 22.2%, p = 0.027), and poor histological grade (71.4% vs. 37.5%, p = 0.039). In conclusion, the cell populations in metastatic nodes revealed DNA pattern which differed from that of primary tumors. The ploidy pattern and SPF in metastatic nodes might be considered as discriminate measure for risk factors in breast cancer patients with positive axillary node.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Liver failure due to ischemia-reperfusion injury, believed to be closely related to the generation of oxygen-free radicals, is a serious problem during liver surgery. Gabexate mesilate, a synthetic protease inhibitor, suppresses the extracellular release of oxygen-free radicals in the microvascular endothelium. To determine its effects on ischemia-reperfusion injury to the liver, we performed experiments with rats. We divided the animals into two ischemia-reperfusion groups: an experimental group, which underwent ischemic injury for 30 minutes, along with the infusion of gabexate mesilate, and a control group, which underwent injury only. Each group was then divided into four subgroups: ischemic injury only and 60-, 120-, and 180-minute reperfusion injury. The test parameters were tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) in serum and superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) in liver and lung tissues. The experimental group had a significantly higher liver SOD and catalase levels and a significantly lower level of liver and lung MDA than the control groups. TNFα levels in the experimental groups were significantly lower during the early phase, but a comparison of IL-6 levels between the two groups yielded no differences. Levels of lung catalase and SOD were not significantly different between the two groups. We concluded that protease inhibitor suppressed liver ischemia-reperfusion injury, and that it was due to an increase of antioxidant or suppression of oxygen-free radicals. The roles of TNFα and IL-6 in liver reperfusion injury were not clear, though TNFα might have had an effect during the early phase. With liver ischemia-reperfusion injury, the mechanism of lung involvement might be different from that of liver involvement.
    Type of Medium: Electronic Resource
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