Disease relevance of Microscopy, Phase-Contrast

• Treatment with human amylin(1-37) resulted in prominent toxicity as assessed by phase-contrast microscopy and quantification of lactate dehydrogenase in the medium [1].
• We now show that the spreading of murine mammary adenocarcinoma LM3 cells was significantly reduced by n-butanol, a PLD and PKC inhibitor, with a maximal inhibition of 54% (p < 0.001) in both the presence and absence of serum, as measured by phase-contrast microscopy [2].
• Evaluation of cellular damage during hypoxia using phase-contrast microscopy, trypan blue exclusion, chromium release, and adherent cell counts showed that EC survived longer with less damage than any of the above cell types [3].
• Presumptive colonies were identified as Campylobacter spp. by phase-contrast microscopy and Gram stain, and they were confirmed by serological latex agglutination [4].
• In a pediatric and in an adult group of patients with hematuria and normal creatinine clearance overnight urine examination was carried out on 2 nonconsecutive days by means of phase contrast microscopy by two independent observers working in two different institutions [5].

High impact information on Microscopy, Phase-Contrast

• Under phase-contrast microscopy, PAF caused contraction of mesangial cells with a dose-response and time-course parallel to that for PGE2 synthesis [6].
• Phase-contrast microscopy revealed that anti-TSP Fab caused a marked decrease in platelet macroaggregates and an increase in microaggregates and nonaggregated single platelets [7].
• The ankyrin-3-positive vesicles appear dark on phase-contrast microscopy [8].
• Cell surface HSPG aligned with microfilament bundles of rat embryo fibroblasts seen by phase-contrast microscopy but was diffuse on transformed rat dermal fibroblasts (16C cells) which lack obvious stress fibers [9].
• [Ca2+]i was estimated by measuring the ratio of fluorescent image pairs (collected at 340- and 380-nm excitation), morphological changes were observed by phase-contrast microscopy, and viability was assessed by trypan blue exclusion [10].

Chemical compound and disease context of Microscopy, Phase-Contrast

• Fluorescence microscopy and 3H-dopamine uptake measurements reveal that the toxicity is selective for dopamine neurons, whereas other neurons and cells in the culture appear normal by phase contrast microscopy [11].
• The non-functioning adrenocortical adenoma cells which were incubated in vitro under ACTH (10 mIU/ml) and angiotensin II (10(-6) M/ml) stimulation, were examined by phase contrast microscopy, transmission and scanning electron microscopy, and the content of cortisol and aldosterone in the culture medium was measured by radioimmunoassay [12].
• The effect of MPP+ on the morphology of C6 glioma cells was observed under phase contrast microscopy; apoptosis of C6 glioma cells were measured by FITC-labeled Annexin V staining and flow cytometry [13].
• On being killed, both bullae were removed and fixed in osmium tetroxide, and prepared of phase-contrast microscopy by the surface preparation technique [14].

Biological context of Microscopy, Phase-Contrast

• Glass adherence and phagocytosis of small particles (latex and carbon black) were demonstrated with phase contrast microscopy [15].
• By immunoblotting, phase-contrast microscopy, and immunolocalization studies we report here that hepatocyte growth factor (HGF) induces a pronounced migratory/scatter phenotype in neonatal hepatocytes in primary culture [16].
• In intact mitotic endothelial cells, chromosomes instantly unfolded as detected by phase contrast microscopy when the salt concentration in the culture medium was increased from 110 to 410 mM NaCl or from 0 to 65 mM MgCl2 [17].
• Cell-permeable ceramide, N-acetyl-D-sphingosine, induced apoptosis of dermal fibroblasts in a dose- and time-dependent manner, which was detected by phase contrast microscopy, fluorescent microscopy, the TUNEL method, flow cytometric analysis, and WST-1 assay [18].
• Cell viability was assessed by trypan blue staining, cell counting, and phase-contrast microscopy [19].

Anatomical context of Microscopy, Phase-Contrast

• Endothelial cells were characterized by phase-contrast microscopy, electron microscopy and the presence of Factor VIII-related antigen [20].
• After incubation with VLDL, massive accumulation of phase refractile (lipid) inclusions were noted by phase contrast microscopy within the normal, but not within the lipoprotein lipase-deficient, macrophages [21].
• METHODS: The binding of spores to ECM proteins and to epithelial cells was carried out using a direct binding assay in microtitre plates and spores were counted by phase contrast microscopy [22].
• Cyclospora oocysts can be detected by phase contrast microscopy, modified acid-fast staining, autofluorescence, and amplification by the polymerase chain reaction [23].
• As observed by phase-contrast microscopy, the response to CaCl2 was characterized by events that occurred in the following temporal sequence: disruption of the sperm rouleaux, the loss of refractility by the apical segment of the sperm acrosome, and detachment of the apical segment from the spermatozoa [24].

Associations of Microscopy, Phase-Contrast with chemical compounds

• Maintenance of normal platelet morphology as determined by phase-contrast microscopy, extent of shape change response, and the size distribution according to the Coulter Counter correlated with recovery in vivo [25].
• The characteristic diameter for the ML resonance compartment measured by NMR for the C6 cells was not significantly different from the one obtained with phase contrast microscopy (1.88 +/- 0.04 micro m from NMR versus 1.37 +/- 0.33 micro m from microscopy) [26].
• The effect of an antitumor antibiotic, neocarzinostatin (NCS), on the formation of microtubular paracrystals (PC) induced by vinblastine sulfate, 10 mug/ml, in HeLa-S3 cells was examined by phase-contrast microscopy [27].
• During the growth-inhibitory period, erythrosin B dye was excluded equally well (greater than 94%) by control and treated cells, and no morphological differences were detected by phase contrast microscopy [28].
• PMB1-induced spores of GW2 do not differ from wild-type spores in morphology by phase-contrast microscopy, dipicolinic acid content, or rate of sedimentation through Renografin gradients [29].

Gene context of Microscopy, Phase-Contrast

• BMP-2 and BMP-4 increased protein synthesis, in agreement with our observation by phase-contrast microscopy of a highly refractile matrix around MC615 cells treated with BMP-2 and -4 [30].
• 6. The aggregating potency of cells was: alphavbeta3/MT1-MMP >alphavbeta3=mock cells, as shown by aggregometry and phase-contrast microscopy [31].
• Morphological phenotype of cultured SHEE cells from the 6th to 30th passages, was examined by phase contrast microscopy, the telomere length was assayed by Southern blot method, and the activity of telomerase was analyzed by telomeric repeat amplification protocol (TRAP) [32].
• EMT was assessed by: morphology under phase-contrast microscopy; Western analysis of cell lysates for expression of mesenchymal phenotypic markers including fibronectin EDA (Fn-EDA), and expression of epithelial phenotypic markers including E-cadherin (E-cad) [33].
• In vitro galectin-8 mediated effects (and the influence of its neutralising antibody) on migration levels of living HCT-15, LoVo, CoLo201, and DLD-1 cells were quantitatively determined by computer assisted phase contrast microscopy [34].

Analytical, diagnostic and therapeutic context of Microscopy, Phase-Contrast

• Cultures were analysed from day 1-12 by phase contrast microscopy and scanning electron microscopy (s.e.m.). Levels of fibrin degradation products (FDP) and tissue plasminogen activator (tPA) accumulating in culture media were quantified by ELISA [35].
• The effects of epidermal growth factor (EGF), cholera toxin (CT), extracellular calcium and 13-cis-retinoic acid on cell growth, morphology, phenotype, and cytodifferentiation were studied using phase-contrast microscopy and indirect immunofluorescence [36].
• Cells at passage #3 were cultured for long term in alpha-minimum essential medium containing 10% fetal bovine serum, antibiotics, and 50 micrograms/ml ascorbic acid, and were then examined using phase-contrast microscopy, histochemistry, transmission electron microscopy, X-ray microanalysis, and electron diffraction [37].
• Aggregation of compound 1 into large supramolecular aggregates was visualized via phase-contrast microscopy and atomic force microscopy [38].
• Apoptosis induced by HMBA was detected by phase-contrast microscopy, flow cytometry, propidium iodide staining and immunocytochemical analysis [39].

References