Bronchoscopy obtaining bronchoalveolar lavage (BAL) fluid and bronchial secretions (BS) and/or high-resolution computed tomography (CT) of the lungs were performed in 33 patients with pulmonary aspergillosis from 1987 to 1992. The sensitivity of BAL fluid or BS for detecting histologically proven fungal disease was 33 and 50%, respectively, whereas positive serologies were only documented in 8% of the cases. CT scans contributed to the early diagnosis of opportunistic fungal pneumonia: characteristic CT signs were found in 16 of 19 episodes. The more frequent use of bronchoscopy and CT scans between 1990 and 1992 compared to 1987-1989 for the differential diagnosis of new pulmonary infiltrates resulted in earlier appropriate treatment. The average introduction of intravenous (i.v.) antifungal therapy after the onset of pneumonia was shifted from 12 to 7 days (p < 0.05). The timely implementation of i.v. antimycotic therapy had a significant impact on survival. Initiation of antifungal treatment later than 10 days after the onset of pneumonia resulted in a mortality of 90%, as opposed to 41% with an earlier start of antimycotics (p < 0.01). The earlier use of appropriate antifungal therapy in the second treatment period improved survival from 33 to 50% (NS). Bronchoscopy and high-resolution CT scans are mutually complementary diagnostic tools and should be performed as early as possible in the course of pneumonia for patients at high risk for aspergillosis.
Summary MicroRNAs (miRNAs) play an important role in cellular differentiation and cancer pathogenesis. This study analysed the expression of 154 human miRNAs in acute myeloid leukaemia (AML) and control samples using a stem‐loop real‐time reverse transcription polymerase chain reaction approach. Global patterns of miRNA expression in AML, normal bone marrow (NBM) and CD34+ progenitor cells allowed correct class predictions similar to whole genome microarray expression analyses that were performed at the same time. At single miRNA species level, MIRN23B was repressed in AML specimens compared to NBM and purified CD34+ haematopoietic progenitor cells. In contrast, the MIRN221/MIRN222 cluster and MIRN34A were expressed at significantly higher levels in AML blasts. Patients with high MIRN221/MIRN222 expression showed low levels of KIT RNA and protein expression but the correlation between kit protein and KIT mRNA was significantly stronger than the correlation of either one with MIRN221/MIRN222. A global analysis between miRNA expression levels and mRNA expression of predicted target genes revealed only weak associations in the majority of miRNA species. Nonetheless, the presence of two or more miRNA binding sites within the mRNA was usually associated with a decrease in mRNA levels. Taken together, these findings provide evidence that specific miRNA expression patterns exist in AML.
RGD-Cy 5.5 combined with novel tomographic optical imaging methods allows non-invasive imaging of tumour-associated alpha v beta(3) expression and may thus be a promising strategy for sensitive evaluation of tumour target expression.
Tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 are proteins with proteinase-inhibiting and cytokine properties. TIMP-1 is active primarily in B cells and B-cell lymphomas, whereas TIMP-2 expression is restricted to T cells. The expression of TIMP-1 and TIMP-2 in lymph nodes from patients with Hodgkin disease (HD) and in Hodgkin-derived cell lines was investigated. In situ hybridization showed TIMP-1 RNA expression in 3% to 80% of Hodgkin/Reed-Sternberg (H/R-S) cells from 14 of 15 patients, with results in one patient being at the lowest detection limit; no expression of TIMP-2 in H/R-S cells; and only weak expression of TIMP-2 in reactive lymphoid tissue. Production of TIMP-1 protein by H/R-S cells was accordingly found on immunohistochemical analysis of lymph nodes from patients with HD. There was only low expression of matrix metalloproteinase (MMP)-2, which is mainly inhibited by TIMP-2; no expression of MMP-1 and MMP-3 in reactive lymphoid tissue; and no expression of these MMPs in H/R-S cells. Thus, TIMP-1 expression in lymph nodes was not correlated with metalloproteinase expression. Five of 7 Hodgkin-derived cell lines expressed TIMP-1 at the protein level. Only one of these cell lines expressed TIMP-2, at the lowest detection limit. TIMP-1 levels in plasma from patients with HD were within the same range as those in plasma from healthy controls. Recombinant human TIMP-1 inhibited induced cell death in Hodgkin-derived cell lines in vitro. TIMP-1 and TIMP-2 inhibited T-cell cytotoxicity against autologous cells presenting tumor-associated antigens and in allogeneic mixed lymphocyte cultures. Thus, TIMP-1, aside from its role in proteinase equilibrium, is an autocrine and paracrine survival factor for H/R-S cells and an immunosuppressive protein expressed in Hodgkin lymphomas.
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