[Progress of lung cytology from 1965. I. Methodology of cytodiagnosis].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Zimmer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Extended trauma causes a failure of T-lymphocyte function due to suppressed interleukin-2 synthesis; however, the role of IL-2 receptor, especially its soluble form (sIL-2R), needs to be further evaluated. It was the objective of the study to assess the kinetics of sIL-2R within different settings of trauma and to define its clinical value and possible predictive role. Three groups of patients with trauma were included in the study. Groups 1 and 2 consisted of multiply injured patients (injury severity score 35 +/- 4 and 32 +/- 4, respectively); burned patients formed group 3 (injury severity score 38 +/- 9). Serum samples were collected at the site of the accident (group 1) and during the posttrauma course in the hospital (group 2, daily; group 3, weekly) and sIL-2R was measured in these samples. sIL-2R was within the normal range in groups 1 and 2, but was significantly increased in group 3. There was no correlation between serum concentrations of this mediator and susceptibility to infectious complications or outcome.
Interactions between bacterial adhesins of lectin type and the oligosaccharide part of immobilised glycoconjugates on the tooth surface are involved in the specific colonisation of teeth. The specificity of the adhesion process is determined by the carbohydrate specificity of the bacterial lectins and the availability of the corresponding glycosylation pattern. On the other hand the same carbohydrate structures can specifically prevent the binding of bacteria by competitively blocking their adhesion, if sufficient amounts of this distinct carbohydrate structure are available in the secretion. Since carbohydrate binding receptors are also involved in the colonisation of tooth surfaces by cariogenic bacteria, it has been suggested that the architecture of the oligosaccharide portion of soluble glycoconjugates in saliva may play an important role as a constitutional host defence factor in the aetiology of dental caries. Characterising the availability of distinct carbohydrate patterns in saliva by using a pattern of well-described lectins in a competitive lectin inhibition assay we show that in children of a population-based sample a high caries susceptibility is associated with a reduced binding inhibition against the lectin peanut agglutinin (PNA). PNA is specific for the presence of terminal galactosyl residues and binds to the same O-glycan fractions as a surface lectin from Streptococcus mutans. The data suggest that a reduced availability of glycosylation patterns of galactosyl residues detected by the lectin PNA may act as an additional host-derived factor for an increased caries susceptibility.
To gain further insight into the process of metastasis, adhesion to endothelial monolayers was compared for a nonmetastatic and a highly metastatic human breast cancer cell line. The parallel plate flow chamber was employed to quantify adhesion using an attachment assay. This assay was carried out at several physiological shear stresses both with and without endothelial TNF-alpha stimulation. At a venular shear stress of 1 dyne cm-2, the nonmetastatic cell line was more adhesive to stimulated endothelial monolayers, while no differences could be noted for resting monolayers. At a lower shear stress of 0.25 dynes cm-2, the highly metastatic cell line was more adhesive to stimulated endothelial monolayers, while the nonmetastatic cell line was more adhesive to resting monolayers. Thus, metastatic potential correlated with attachment only at low shear stresses and following endothelial stimulation. These results emphasize the importance of studying cancer cell adhesion under multiple physiological flow conditions. Furthermore, these results indicate that adhesion of these two cell lines may be controlled by two different mechanisms. Antibody blocking experiments of adhesion molecules on the endothelial cells confirmed that adhesion of the nonmetastatic cell line was mediated by E-selectin expressed on the endothelial cells and adhesion of the highly metastatic cell line was mediated by both E-selectin and VCAM-1 expressed on the endothelial cells.
Monocyte/T-cell interactions play a critical role in the systemic response to infection. Distinct patterns of cytokines are produced by two different types of T-helper cells (Th). Th1 cells secrete interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), whereas Th2 cells produce IL-4, IL-5, IL-6, IL-10, and IL-13. In volunteers systemic endotoxin administration initiates many features of gram-negative sepsis including cytokine release, but the patterns (i.e., Th1/Th2 patterns) have not yet been studied. In this institutional review board-approved study we investigated the effect of an intravenous bolus of endotoxin from Escherichia coli (4 ng/kg body weight) on the Th1/Th2 response in four female and four male volunteers (mean age 27.1 +/- 0.8 years). Plasma cytokine levels for IL-2, IL-4, IL-10, IL-12, and IFN-gamma and heart rate, mean arterial pressure, temperature, white blood cell, and differential blood count were determined before and hourly for 5 hours after endotoxin administration. All volunteers had tachycardia, decreased mean arterial pressure, fever, and leukocytosis. IL-10 was significantly (p < 0.05) elevated (9.4 +/- 3.9 pg/ml vs 60.9 +/- 19.3 pg/ml) 3 hours after endotoxin was administered, whereas IL-2 levels were decreased (69 +/- 26 U/ml vs 30.6 +/- 14.9 U/ml). IL-4 and IFN-gamma were not detectable in plasma. No changes were seen in the plasma levels of IL-12. Systemic responses did not correlate with changes in cytokine levels. Cytokine patterns found in this study suggest that after low-dose endotoxin administration the T-cell immune response is shifted towards the Th2 cell type response. This early shift towards a Th2 cell response may contribute to the depressed cell-mediated immune response associated with sepsis.