Correlation function of finite two-dimensional superconductors.
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Biomedical subjects
Publications and source records attributed to J Appel.
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A total of 171 pleural needle biopsies were carried out in 123 patients with pleural effusion. The sensitivity of the method proved to be 51% for malignant diseases and 75% for tuberculotic pleurisy, respectively. Performing biopsy simultaneously with the cytological examination of the pleural fluid, malignancy was proved only by needle biopsy in 20% of the patients, while cytology was found negative in these cases. Simultaneously performed thoracocentesis and pleural needle biopsy is suggested.
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The structure of epithelial mast cells obtained by bronchial biopsy from asthmatic patients reveals characteristic qualitative and quantitative features. Great amount of partly or completely depleted mast cells can be observed in active asthmatic patients, indicating the liberation of bronchoconstrictive mediators. After a two months treatment with inhalative steroid (budesonide) the process of degranulation slows down, the number of depleted mast cells decreases. Parallel with the above described phenomenon, the number of dyspneic attacks, as well as the necessity of other antiasthmatic drugs show a significant decrease. However, in this patient material, during the treatment period, airway hyperreactivity, detected by bronchial provocation, failed to show any remarkable change.
Heparin-induced thrombocytopenia and thrombosis is associated with a significant incidence of morbidity and mortality. Prompt recognition of this complication and immediate withdrawal of heparin therapy are imperative. This report describes a case of heparin-induced thrombosis and thrombocytopenia with major vascular insufficiency of the extremities. This is the first reported instance of the use of intravenous streptokinase for the treatment of heparin-induced venous thrombosis.
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Pediococci, vancomycin-resistant gram-positive cocci, have been isolated from human specimens, but an association with clinical illness has not been established. Clinical and epidemiologic data were obtained on nine patients who had Pediococcus acidilactici isolated from blood. Patients were eight elderly adults with complicated medical problems and one infant with congenital jejunoileal atresia. Seven patients were hospitalized before P. acidilactici was isolated. Eight had received multiple antibiotics; however, only two had received vancomycin. In all cases there was a delay in correct bacterial identification, and the significance of the isolate was uncertain. There was no clearly identified syndrome associated with P. acidilactici bacteremia. All eight adults had fever and six had pneumonia potentially attributable to other causes. The findings underscore the importance of proper identification of vancomycin-resistant gram-positive cocci. P. acidilactici may be an opportunistic pathogen in severely compromised hosts; however, further observations are necessary to clarify its role in human disease.
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The effects of several noncollagenous matrix proteins on hydroxyapatite formation and growth were studied in a dynamic collagen gel system. In this system growth plate proteoglycan aggregates at concentrations of 1-10 micrograms/ml were effective inhibitors, desulfated aggregates from brachymorphic mice were less effective. Phosphophoryn at 1-100 micrograms/ml had no effect on formation; 60-120 micrograms/ml retarded mineral growth. Type X collagen at concentrations of 50-300 micrograms/ml had no effect on formation or growth.
Specimens from the lung obtained during the treatment of spontaneous pneumothorax revealed a hitherto unknown histological phenomenon characterised by a histiocytic, inflammatory interstitial pulmonary tissue containing gas. By following the course of the gas an intracellular pathogen could be identified in the macrophages. Its shape resembled that of micrococci, ist size was between 2-4 microns. The ultrastructure within the pathogen suggested gas formation. In these cases the origin of the pneumothorax was attributed to the aerogenous microorganism that had induced a phagocytic inflammation in the pulmonary tissue.
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The mitochondrial gene for the cytochrome b of Complex III has been cloned from a mouse L-cell mutant with increased resistance to 2-n-heptyl-4-hydroxyquinoline-N-oxide and other inhibitors which block reactions at the b562 heme group. Nucleotide sequencing revealed that this gene contained a G:A transition on the coding strand at position 14,830. At the amino acid level, this mutation results in the substitution of an aspartic acid residue for a conserved glycine at position 231 of cytochrome b. Based upon current models for the secondary structure of cytochrome b, the altered amino acid lies in close proximity to one of the invariant histidine residues involved in binding the heme groups. Combining this result with the previous biochemical studies of this mutant, we hypothesize that the insertion of this highly charged side chain alters the conformation around the b562 heme group such that 2-n-heptyl-4-hydroxyquinoline-N-oxide and the other inhibitors of this group have reduced access to the inhibitor binding domain.
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Results of electron microscopic examinations of the pulmonary alveolar macrophage in healthy nonsmokers, smokers and in patients with proteinosis, hard metal coniosis and sarcoidosis are reviewed. Authors have carried out the staining of the acid phosphatase and peroxydase enzymes as well. Ultrastructural alterations in the different cases were very characteristic, but the cytochemical results in the macrophages from sarcoidosis are not pathognomonic.