Variet?ten des Brustbeines

Ohne ZusammenfassungMit 12 Abbildungen im Text und 6 Figuren auf den Tafeln 3/6.     

Paramecium calcium channels are blocked by a family of calmodulin antagonists.

Although the voltage-sensitive Ca channel present in Paramecium has been subjected to detailed physiological and genetic analysis, no organic ligands have been described that block this channel with high affinity and that ultimately can be used to identify channel components. Based on a previous observation that the naphthalene sulfonamide calmodulin antagonist W-7 can block Paramecium Ca channels at high concentration, we have synthesized analogs of W-7 that block these channels at concentrations of less than 1 microM. The effectiveness of these compounds was tested both by a sensitive behavioral assay and on Ca channels that had been incorporated into planar lipid bilayers. Despite the fact that these compounds are effective Paramecium calmodulin antagonists, two independent lines of evidence suggest that W-7 and its analogs block the Ca channel by a mechanism that is independent of their action on calmodulin. In addition, the sensitivity to W-7 or dihydropyridines of Ca channels present in a number of eukaryotic phyla has been used to identify similarities in Ca channels from widely diverse organisms. It appears that the pharmacological specificity provides a means to group Ca channels.     

Regional differences in calcium-release channels from heart.

The heart is a heterogeneous tissue composed of several cell types tailored for specialized functions. We found that intracellular channels also exhibit regional specialization. In cardiac and skeletal muscle these channels are called the calcium-release channel and are identified by activation with either calcium or caffeine and inhibition by the hexavalent cation ruthenium red. The calcium-release channel of the sarcoplasmic reticulum from the interventricular septum has a smaller conductance (31 pS vs. 100 pS) and has longer open and closed times when compared with the channel from left-ventricular free wall. An additional calcium-permeable channel with an even smaller conductance (17 pS) was found in the septum, and this channel is similar to the inositol 1,4,5-trisphosphate-gated channel from smooth muscle and different from the calcium-release channel (ryanodine receptor) from skeletal and cardiac muscle. The inositol 1,4,5-trisphosphate-activated channel may be derived from specialized conducting tissue that is relatively abundant in the septum, whereas the other calcium-release channels may be derived from regionally specialized myocardial cells in the septum and free wall.     

A mixing model for polychlorinated dibenzo-p-dioxins and dibenzofurans in surface sediments from Newark Bay,New Jersey using polytopic vector analysis

The identity and relative contributions of various sources of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) to recently deposited sediments collected in Newark Bay and its major tributaries were determined using polytopic vector analysis (PVA), a multivariate statistical technique relatively new in the chemometric literature. The concentrations of 2,3,7,8-substituted PCDD/Fs were assayed in eighty-one surface and near-surface sediment samples collected from the Passaic River, Hackensack River, Arthur Kill, Elizabeth River, Kill Van Kull, Port Elizabeth, and Port Newark navigation channels and Robins Reef, which is located in New York Harbor. PVA modeling revealed five predominant 2,3,7,8-substituted PCDD/F fingerprint patterns in geographically plausible distributions throughout the estuary. This was consistent with the current understanding of hydrodynamic and sedimentation conditions reported in the literature for Newark Bay. Three patterns contained 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), which is alleged to originate from a single industrial source on the lower Passaic River. One of the fingerprints containing 2,3,7,8-TCDD was present in moderate proportions (10–20%) in surface sediments near the site, but was generally observed in low abundance (<5%) elsewhere in the estuary. A fingerprint pattern characteristic of PCDD/F profiles in effluents from municipal sewage and waste water treatment plants was widely distributed in the estuary, but reached its highest relative proportions in the Elizabeth River. A third fingerprint pattern was highest in the Arthur Kill and lower Passaic River and closely matched the residue patterns found in several types of combustion sources. A fourth finger-print pattern in Hackensack River and lower Passaic River sediment matched the PCDD/F profile reported in PCB Aroclor^® formulations. A fifth fingerprint pattern matched the profile in recycled pulp and paper mill effluents and was highest in Kill van Kull and upper Passaic River sediment. The majority of PCDD/Fs in sediment from Reaches B, C, and D of Port Newark and Port Elizabeth were attributable to sediments transported via the Arthur Kill and the Kill Van Kull. These results are consistent with those previously reported using principal components analysis, which indicated that 2,3,7,8-substituted PCDD/F patterns in the sediments of Newark Bay are consistent with discharges from multiple sources.     

Maculopapular eruption with enlarged macrophages in eight patients receiving G-CSF or GM-CSF

In the last years, granulocyte and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF) are being increasingly used and several cutaneous eruptions have been reported in relation to these treatments. In 1991 Horn et al. described three patients with maculopapular eruption that paralleled the time of infusion of GM-CSF. Two of the cases showed an increase in the number and size of macrophages in the biopsy specimen. Since then, several cases have been reported showing this histopathological alteration that has been considered characteristic of reaction to G-CSF or GM-CSF. Although maculopapular eruption with enlarged macrophages can appear after chemotherapy treatment, we have found that the presentation of this eruption after the beginning of cytokine treatment is suggestive of the involvement of G-CSF and GM-CSF in the eruption. We described eight cases of patients treated with G-CSF or GM-CSF that developed maculopapular eruptions with enlarged macrophages.