ABSTRACT
This study is devoted to the experimental and theoretical investigation of aerodynamic drop breakup phenomena. We show that the phenomena of drop impact onto a rigid wall, drop binary collisions, and aerodynamic drop deformation are similar if the correct scaling is applied. Then we use observations of the deforming drop to estimate the evolution of the film thickness of the bag, the value that determines the size of the fine child drops produced by bag breakup. This prediction of film thickness, based on film kinematics, is validated for the initial stage by direct drop thickness measurements and at the latest stage by the data obtained from the velocity of hole expansion in the film. It is shown that the film thickness correlates well with the dimensionless position of the bag apex.
ABSTRACT
A flow chamber has been constructed to use giant liposomes (diameter 5-50 microns) as model membranes for immunological studies and other experiments involving the interaction with water-soluble compounds. As an example of immunological importance, the insertion of purified K-antigen from Escherichia coli K1 has been studied. Despite its large hydrophilic part (poly-alpha-2,8-NeuAc), which is capped at its potential reducing end with phosphatidic acid acting as a lipid anchor group, this water-soluble material is readily incorporated into liposomal membranes of dimyristoylphosphatidylcholine (DMPC). The incorporation has been proven by immunofluorescence using a FITC-labeled monoclonal anti-K1-IgG. Without the lipid residue, however, no binding of poly-alpha-2,8-NeuAc to the liposomes has been observed. This could be shown by using colominic acid, an oligomeric form of alpha-2,8-NeuAc with free reducing ends instead of purified K1-antigen. The possibility for further manipulation of this model system has been shown by using a poly-alpha-2,8-NeuAc cleaving enzyme (endoneuraminidase). The function of the endoneuraminidase has been proven by showing no binding of the antibody after enzyme treatment of K1-bearing liposomes as well as by rapid loss of fluorescence of a previously bound FITC-antibody.
Subject(s)
Antigens, Bacterial/isolation & purification , Antigens, Surface/isolation & purification , Escherichia coli/analysis , Liposomes/immunology , Antibodies, Monoclonal/biosynthesis , Antigens, Bacterial/immunology , Antigens, Surface/immunology , Dimyristoylphosphatidylcholine , Escherichia coli/immunology , Fluorescent Antibody Technique , Immunoglobulin G/analysis , Membrane Lipids/immunology , Microscopy, Phase-Contrast , Models, Biological , Neuraminidase/isolation & purification , Solubility , WaterABSTRACT
Histological and bacteriological findings in comparison to clinical data concerning intubation for 38 dead premature infants and newborns were studied to elucidate conditions complicating intratrachial intubation at the laryngeal level. The larynx was intact in 3 cases. Slight lesions of mucosa (epithelabrasion, hemorrhage) were found in 13, moderately severe lesions (necrosis of epithelium, ulcers, pseudomembranes) in 11, and severe lesions (deep necrosis, perichondritis with sceletisation) in 10 cases. 1 case showed a stage of regeneration. The narrow passage between the two processus vocales is a site of predilection for tubus-induced lesions, the epithelium bein immediately adjacent to the cartilage. Successful bacteriological demonstration of the infectious agent correlated with the rising degree of mucosal lesions, and increasing duration of intubation. 3 cases, however, already had severe lesions after short-time-intubation. Formal and causal pathogenesis are described. Essential causes are: trauma of intubation, irritation by the tubus in situ, duration of intubation, and infection. Regenerative power of the infantile laryngeal mucosa is strong. Permanent lesions may occur as scarred stenosis. Careful indication, accurate and careful technology of intubation, choice of the smallest possible diameter of tubus, good care for the tubus, and generous prophylaxis against infections are to be demanded.
