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Biomedical subjects

E Eichhorn

Publications and source records attributed to E Eichhorn.

6 recordsLinked to original sources
PubMed1998

Differences in cellular infiltrates in the adenoid of allergic children compared with age- and gender-matched controls.

BACKGROUND: Allergic sensitization of the airways occurs in the mucosa of the shock organ, or in the lymphatic stations draining these structures. The lymphatic structure closest to the nasal mucosa is the adenoid. OBJECTIVES: The objective of this study was to find evidence for our hypothesis that allergic sensitization can occur in the adenoid. Of special interest, in this context are cell types involved in antigen-allergen presentation (e.g. Langerhans cells) and effector cells of allergic disease. METHODS: In this study cellular infiltrates in adenoids of 16 allergic patients and 16 age- and gender-matched controls were evaluated. The number of cells positive for CD1a, CD4, CD8, CD-68, chymase, tryptase, IgE, MBP and cells positive for interleukin (IL)-4 were determined using immunohistochemical staining techniques. The epithelium, follicles and the interfollicular spaces were evaluated separately. RESULTS: When comparing the two groups a significant increase in cells positive for CD1a was found in interfollicular spaces of the allergic group (P = 0.008). CD1a+ cells in the follicular space and eosinophils in the interfollicular space showed a trend to be more numerous in the allergic group (P = 0.02 and P = 0.05, respectively). The other cell types investigated did not show significant differences between the groups. CONCLUSIONS: The results of this study show for the first time that cells involved in allergic sensitization and allergic disease differ in the adenoid of allergic children compared with controls. These findings support our hypothesis that allergic sensitization takes place in the adenoid. Furthermore, this study confirms that CD1a+ (Langerhans) cells are involved in allergic disease.

Adenoids↗
PubMed1997

Characterization of alpha-ketoglutarate-dependent taurine dioxygenase from Escherichia coli.

The Escherichia coli tauD gene is required for the utilization of taurine (2-aminoethanesulfonic acid) as a sulfur source and is expressed only under conditions of sulfate starvation. The sequence relatedness of the TauD protein to the alpha-ketoglutarate-dependent 2,4-dichlorophenoxyacetate dioxygenase of Alcaligenes eutrophus suggested that TauD is an alpha-ketoglutarate-dependent dioxygenase catalyzing the oxygenolytic release of sulfite from taurine (van der Ploeg, J. R., Weiss, M. A., Saller, E., Nashimoto, H., Saito, N., Kertesz, M. A., and Leisinger, T. (1996) J. Bacteriol. 178, 5438-5446). TauD was overexpressed in E. coli to approximately 70% of the total soluble protein and purified to apparent homogeneity by a simple two-step procedure. The apparent Mr of 81,000 of the native protein and the subunit Mr of 37,400 were consistent with a homodimeric structure. The pure enzyme converted taurine to sulfite and aminoacetaldehyde, which was identified by high pressure liquid chromatography after enzymatic conversion to ethanolamine. The reaction also consumed equimolar amounts of oxygen and alpha-ketoglutarate; ferrous iron was absolutely required for activity; and ascorbate stimulated the reaction. The properties and amino acid sequence of this enzyme thus define it as a new member of the alpha-ketoglutarate-dependent dioxygenase family. The pure enzyme showed maximal activity at pH 6.9 and retained activity on storage at -20 degrees C for several weeks. Taurine (Km = 55 microM) was the preferred substrate, but pentanesulfonic acid, 3-(N-morpholino)propanesulfonic acid, and 1,3-dioxo-2-isoindolineethanesulfonic acid were also desulfonated at significant rates. Among the cosubstrates tested, only alpha-ketoglutarate (Km = 11 microM) supported significant dioxygenase activity.

Amino Acid Sequence↗
PubMed1986

Effects of lithium carbonate on human calcium metabolism.

Serum calcium and immunoreactive parathyroid hormone levels increase within the normal range in 80% of patients during the first four weeks of lithium carbonate administration and may rise above normal in 10% after long-term therapy. Since the lithium ion in vitro makes the parathyroid cell less sensitive to calcium, and since several lithium carbonate-treated patients with parathyroid adenomas have been described, it has been suggested that the lithium ion can stimulate parathyroid growth. The data are inconclusive, however, since the adenomas could be sporadic and there has been no direct proof of increased parathyroid mass or biologic activity. Based on the available studies, we have formulated a reasonable scheme for monitoring calcium metabolism during lithium carbonate treatment. Proper treatment of hypercalcemic lithium carbonate-treated patients remains uncertain, but we have outlined some tentative management guidelines.

Adult↗