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排序方式: 共有898条查询结果,搜索用时 15 毫秒
1.
M Engelhardt P Bast N Jeblink W Lauer A Popovic H Eufinger M Scholz A Christmann A Harders K Radermacher K Schmieder 《Minimally invasive neurosurgery》2006,49(2):98-103
This study was performed to evaluate the surgical strategy in patients with calvarial tumours, in order to design and modify a robot-assisted trepanation system. A total of 75 patients underwent craniectomy for the treatment of calvarial tumours during the 10-year period from 1993 to 2002. The patients' complaints, the size, location and histology of the tumour, and the various cranioplasty techniques used were analysed retrospectively. In a second procedure several craniectomies at typical locations according to the study's results were performed in a laboratory setting using a hexapod robotic tool, constructed at the Helmholtz-Institute, RWTH Aachen University, and plastic model heads. The workflow was documented and the reproducibility and the accuracy of the procedure were registered. A total of 83 surgical procedures were performed on 75 patients. The majority (87 %) of lesions treated surgically were located in the frontal, temporal and anterior parts of the parietal region. Histological examination revealed benign lesions in 66 % of the patients and dural involvement in 46 %. According to these results craniectomies were performed using the robotic system. Mean positioning accuracy of the robotic system while milling was 0.24 mm, with a standard deviation of 0.04 mm, and maximum error under 1 mm. Craniectomies leaving a 1-mm layer of the tabula interna intact to ensure a healthy dura were performed in several regions successfully. The majority of calvarial tumours, requiring surgical treatment in our patients, were located in cosmetically relevant areas in which drilling can be carried out with the robotic trepanation system. Consequently, the surgical approach had to be planned carefully in order to achieve a good cosmetic outcome. 相似文献
2.
3.
Occurrence of the t(2;5)(p23;q35) in non-Hodgkin's lymphoma 总被引:9,自引:3,他引:6
Weisenburger DD; Gordon BG; Vose JM; Bast MA; Chan WC; Greiner TC; Anderson JR; Sanger WG 《Blood》1996,87(9):3860-3868
Primary CD30(Ki-1)-positive anaplastic large-cell lymphoma (ALCL) is considered by some to be a distinct clinicopathologic entity associated with the t(2;5) (p23;q35). However, the specificity of t(2;5) for ALCL has not been carefully studied. Therefore, we performed a detailed analysis of all cases of ALCL with abnormal cytogenetics results in the Nebraska Lymphoma Study Group registry, as well as all other cases of non-Hodgkin's lymphoma with t(2;5) in the registry. We found the t(2;5) in only five of 10 cases of ALCL, four of whom were young patients. However, we also found the t(2;5) in 11 other cases of nonanaplastic lymphoma, including eight children with typical peripheral T-cell lymphomas of various types. The t(2;5) was also found in three older adults with B-cell lymphomas of various types. Thus, the t(2;5) was not specific for CD30+ ALCL. However, t(2;5) may define a clinicopathologic entity in children and young adults characterized by variable morphologies with a T-cell or indeterminate phenotype, CD30-positivity, nodal disease with frequent extranodal involvement, advanced stage, and an excellent response to therapy, including bone marrow transplantation for relapsed disease. The clinical relevance of the t(2;5) in older patients requires further study. 相似文献
4.
BACKGROUND. Although the ascites of patients with ovarian cancer has been reported to contain immunosuppressive factors, the identity and source of this activity has not been determined. Previously, the authors showed that conditioned media from two of four epithelial ovarian cancer cell lines inhibits proliferation of mitogen-stimulated human lymphocytes. The physical characteristics of the inhibitory substance are unlike those of peptide growth factors but closely resemble those of fibronectin. METHODS AND RESULTS. In the current study, it was found that the two ovarian cancer cell lines that produce the inhibitory substance have more fibronectin on the cell surface and secrete significantly more immunoreactive fibronectin into their culture media than the other two ovarian cancer cell lines. In addition, the immunosuppressive activity was bound to a gelatin-Sepharose affinity column, known to bind fibronectin. Finally, in ascites from 20 patients with advanced epithelial ovarian cancer, fibronectin levels correlated with the ability to inhibit proliferation of lectin-stimulated lymphocytes (P < 0.001). CONCLUSIONS. Fibronectin is produced by some ovarian cancer cell lines and acts to inhibit proliferation of mitogen-stimulated lymphocytes. Additional studies are needed to clarify the role of fibronectin in ovarian cancer. 相似文献
5.
Determination of the growth fraction in monoclonal gammopathy with the monoclonal antibody Ki-67 总被引:3,自引:0,他引:3
Henk M. Lokhorst Saskia E. Boom Wim Terpstra Paul Roholl Johannes Gerdes Bert J. E. G. Bast 《British journal of haematology》1988,69(4):477-481
The monoclonal antibody Ki-67 reacts with a nuclear antigen that is present only in proliferating cells. The proportion of Ki-67 positive cells may therefore serve as a reliable measurement for the growth fraction in normal and neoplasmic cell populations. We have tested the significance of the MoAb Ki-67 in the classification of monoclonal gammopathy and compared the results with the plasma cell labelling index. In benign monoclonal gammopathy the percentage of Ki-67 positive plasma cells (median 1.6%) was significantly lower than in untreated multiple myeloma (median 9.6). Among the patients with more than 10% Ki-67 positive plasma cells there were some very short survivors. The largest growth fractions (median 41.8%) were found in patients with relapsing multiple myeloma indicating here a different growth pattern more resembling the high-grade lymphomas. A linear correlation between the proportion of Ki-67 positive plasma cells and the labelling index was not found. Determination of the plasma cell growth fraction with the monoclonal antibody Ki-67 in monoclonal gammopathy may help to discriminate benign monoclonal gammopathy from multiple myeloma and will probably identify a subgroup of multiple myeloma patients with a poor prognosis, including those with relapsing multiple myeloma. 相似文献
6.
John M. H. de Klerk Bernard A. Zonnenberg Alfred D. van het Schip Aalt van Dijk Shiuw H. Han Jacques M. S. R. Quirijnen Geert H. Blijham Peter R van Rijk 《European journal of nuclear medicine and molecular imaging》1994,21(10):1114-1120
Rhenium-186 hydroxyethylidene diphosphonate (186Re-HEDP) has been used for the palliative treatment of metastatic bone pain. A phase 1 dose escalation study was performed using 186Re-HEDP Twenty-four patients with hormone-resistant prostate cancer entered the study. Each patient had at least four bone metastases and adequate haematological function. Groups of at least three consecutive patients were treated with doses starting at 1295 MBq and increasing to 3515 MBq (escalated in increments of 555 MBq). Thrombocytopenia proved to be the dose-limiting toxicity, while leucopenia played a minor role. Early death occurred in one patient (10 days after administration) without clear relationship to the 186Re-HEDP therapy. Transient neurological dysfunction was seen in two cases. Two patients who received 3515 MBq 186Re-HEDP showed grade 3 toxicity (thrombocytes 25–50 × 109/1), defined as unacceptable toxicity. After treatment alkaline phosphatase levels showed a transient decrease in all patients (mean: 26% ± 10% IUA; range: 11%–44%). Prostate-specific antigen values showed a decline in eight patients, preceded by a temporary increase in three patients. From this study we conclude that the maximally tolerated dose of 186Re-HEDP is 2960 MBq. A placebo-controlled comparative study on the efficacy of 186Re-HEDP has been initiated. 相似文献
7.
Prof. Dr. Bernhard Schmitt Prof. Dr. Michael Albani Priv.-Doz. Dr. Thomas Bast Prof. Dr. Ulrich Brandl Prof. Dr. Rudolf Korinthenberg Prof. Dr. Gerhard Kurlemann Prof. Dr. Bernd Neubauer Prof. Dr. Ulrich Stephani Dr. Markus Wolff 《Zeitschrift für Epileptologie》2007,20(3):113-119
Zusammenfassung
Der richtige Zeitpunkt für das Absetzen der Antiepileptika (AE) im Kindesalter ist unbekannt. Anl?sslich ihrer Jahrestagung
haben die Mitglieder des K?nigsteiner Arbeitskreises (KA) eigene und publizierte Absetzstrategien diskutiert. Da Studien zu
diesem Thema rar und widersprüchlich sind, wurde beschlossen, die Diskussionsergebnisse im Sinne einer Meinungs?u?erung zu
publizieren.
Bei Neugeborenen besteht übereinstimmung, AE innerhalb von 2 bis 12 Wochen nach dem letzten Anfall abzusetzen. Bei BNS-Epilepsie
wird Vigabatrin nach 6 bis 12 und Sultiam nach 6 bis 36 Monaten abgesetzt. Nach erfolgreicher Steroidtherapie setzt die Mehrheit
des KA die AE-Therapie für zwei Jahre fort. Für die Rolando-Epilepsie sind 1 bis 3 Jahre Anfallsfreiheit ausreichend, auch
wenn fokale Spike-Waves persistieren. Im Falle einer symptomatisch fokalen Epilepsie ist die Grunderkrankung mitentscheidend
für das Absetzen. Die Behandlung der Absencen-Epilepsie kann nach zwei Jahren beendet werden, w?hrend bei myoklonisch- astatischer
Epilepsie meist eine 2- bis 5-j?hrige Anfallsfreiheit vorausgesetzt wird. Konsens besteht darüber, dass die Juvenile- Myoklonus-Epilepsie
ein sehr hohes Rückfallrisiko birgt. Dennoch ziehen einzelne neurop?diatrische Mitglieder einen Absetzversuch nach 2- bis
3-j?hriger Anfallsfreiheit in Betracht. Die überwiegende Mehrheit des KA führt aber bei gesicherter Diagnose keinen Absetzversuch
durch. Bezüglich der Absetzgeschwindigkeit wird ein langsames (3 bis 12 Monate) Ausschleichen favorisiert. Nur zwei Mitglieder
praktizieren ein rascheres Absetzen (<3 Monaten). Das EEG spielt für die Entscheidung eine untergeordnete Rolle und bleibt
auf bestimmte Epilepsieformen (z. B. Absencen-Epilepsie) beschr?nkt.
Das vorliegende Papier gibt die Meinung des KA wieder und eignet sich nicht im Sinne einer Leitlinie. Für die Entscheidung
AE abzusetzen, ist immer eine individuelle Abw?gung von Grunderkrankung, Epilepsieform und psychosozialen Umst?nde erforderlich.
相似文献
8.
S Wu K Rodabaugh O Martinez-Maza J M Watson D S Silberstein C M Boyer W P Peters J B Weinberg J S Berek R C Bast 《American journal of obstetrics and gynecology》1992,166(3):997-1007
OBJECTIVE: We investigated whether monocyte-derived factors could stimulate the growth of ovarian cancer cells. STUDY DESIGN: Human peripheral blood monocytes or human monocyte-like cell lines THP-1 and U-937 were cultured with or without macrophage colony-stimulating factor, lipopolysaccharide, or phorbol myristate acetate. Culture supernatants or recombinant cytokines were assayed for growth stimulation of ovarian cancer cell lines by tritium-thymidine incorporation and direct cell counts followed by statistical analysis with Student t test. RESULTS: Conditioned medium from peripheral blood monocytes or from THP-1 or U-937 cells stimulated ovarian cancer cell growth. Interleukin-1 alpha, tumor necrosis factor-alpha, and interleukin-6 also stimulated ovarian cancer cell growth, whereas macrophage, granulocyte, and granulocyte-macrophage colony-stimulating factor did not. Concentrations of tumor necrosis factor, interleukin-1, and interleukin-6 in conditioned medium could not account for all the growth stimulation, and activity remained after neutralization of tumor necrosis factor, interleukin-1, and interleukin-6 with antibodies. CONCLUSIONS: Interleukin-1, interleukin-6, tumor necrosis factor, and additional monocyte factor(s) could provide paracrine growth stimulation when monocytes are attracted to ovarian cancers that produce macrophage colony-stimulating factor. 相似文献
9.
Robert C Bast Hans Lilja Nicole Urban David L Rimm Herbert Fritsche Joe Gray Robert Veltri George Klee Andrew Allen Nam Kim Steven Gutman Mark A Rubin Andrew Hruszkewycz 《Clinical cancer research》2005,11(17):6103-6108
A group of investigators met at a Specialized Programs of Research Excellence Workshop to discuss key issues in the translation of biomarker discovery to the development of useful laboratory tests for cancer care. Development and approval of several new markers and technologies have provided informative examples that include more specific markers for prostate cancer, more sensitive tests for ovarian cancer, more objective analysis of tissue architecture and an earlier indication of response to treatment in breast cancer. Although there is no clear paradigm for biomarker development, several principles are clear. Marker development should be driven by clinical needs, including early cancer detection, accurate pretreatment staging, and prediction of response to treatment, as well as monitoring disease progression and response to therapy. Development of a national repository that uses carefully preserved, well-annotated tissue specimens will facilitate new marker development. Reference standards will be an essential component of this process. Both hospital-based and commercial laboratories can play a role in developing biomarkers from discovery to test validation. Partnering of academe and industry should occur throughout the process of biomarker development. The National Cancer Institute is in a unique position to bring together academe, industry, and the Food and Drug Administration to (a) define clinical needs for biomarkers by tumor type, (b) establish analytic and clinical paradigms for biomarker development, (c) discuss ways in which markers from different companies might be evaluated in combination, (d) establish computational methods to combine data from multiple biomarkers, (e) share information regarding promising markers developed in National Cancer Institute-supported programs, and (f) exchange data regarding new platforms and techniques that can accelerate marker development. 相似文献