Über das Aceri-Fraxinetum als vikariierende Gesellschaft des Galio-Carpinetum am Rande der bayerischen Alpen

Zusammenfassung Das Aceri-Fraxinetum der Saalachauen und ähnlicher Tallagen gliedert sich in verschiedene Phasen und Subassoziationen. Als Grund für seine Anwesenheit inmitten eines Fagion-Gebietes wird die Tallage mit ihren lokalklimatischen Eigenarten, vor allem Spätfrost, wahrscheinlich gemacht. Die Assoziation stellt damit eine Vikariante des Eichen-Hainbuchenwaldes dar, der anderwärts eine ähnliche Rolle spielt. Sie ersetzt diesen in kühlen, niederschlagsreichen Tallagen Südbayerns. Eine Parallelerscheinung ist das Ausklingen des Eichen-Hainbuchenwaldes in Skandinavien, wo dieser ebenfalls von eschen- und bergulmenreichen Waldgesellschaften abgelöst wird. In der Eichen-Mischwaldzeit, also vor Einwanderung der Buche, waren dem Aceri-Fraxinetum ähnliche Gesellschaften auf geeigneten Böden in Berglagen allgemein verbreitet. Synsystematisch stellt das Aceri-Fraxinetum die typische Assoziation des Tilio-Acerion-Verbandes dar.

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Summary The Aceri-Fraxinetum of the flood plain of the Saalach and of resembling valley sites is divided in different phases and subassociations. Its presence amidst the area of the Fagion-alliance is probably caused by the valley site with its peculiarities of local climate, especially late frosts. By this the association represents a vicariad of the oakhornbeam-woods, which plays a similar role in places elsewhere. The Aceri-Fraxinetum is replacing the oakhornbeam-woods in valley sites of southern Bavaria, which are cool and rich in precipitation.A parallel appearance is the intermission of the oak-hornbeam-woods in Scandinavia, where, too, it is detached by wood communities rich in ash and mountainous elm.

     

Slow oxygen release on the first two flashes in chemically stressed Photosystem II membrane fragments results from hydrogen peroxide oxidation

Flash-induced amperometric signals were measured with a Joliot-type O₂ rate electrode in spinach Photosystem II (PS II) membrane fragments exposed to very low concentrations of added hydroxylamine or hydrogen peroxide. In both cases anomalous O₂ signals were observed on the first two flashes, and oscillating four-flash patterns were observed on subsequent flashes. The anomalous signals were eliminated in the presence of catalase but not EDTA. The rise times of the O₂-release kinetics associated with the anomalous signals were slow (ca. 20 ms with NH₂OH and ca. 120 ms with H₂O₂) compared to the kinetics of O₂ release on subsequent flashes and in control membranes (3–6 ms). It is proposed that when the intact PS II O₂-evolving complex is perturbed with small concentrations of added reductant, H₂O₂ can gain access and bind to the complex. Bound H₂O₂ can then reduce lower S states in some centers leading to anomalous O₂ signals on the first two flashes. A model is presented to explain both types of anomalous O₂ production. Oxygen observed on the third and subsequent flashes is due to the normal photosynthetic O₂-evolution process arising from the S₃-state. Anomalous O₂ production could be a protective mechanism in PS II centers subjected to stress conditions.Abbreviations DCIP 2,6-dichlorophenolindophenol - EDTA ethylenediaminetetraacetic acid - MES 4-morpholine-ethanesulfonic acid - OEC oxygen-evolving complex - PS II Photosystem II - Y_i O₂ flash yield on the i^th flash - Y_ss steady-state O₂ flash yield level in algae, chloroplasts, or thylakoids after flash-driven S-state oscillations have been damped Formerly, the Solar Energy Research Institute and operated by the Midwest Research Institute for the US Department of Energy under Contract DE-AC-02-83CH10093. Government and MRI retain non-exclusive, royalty-free license to publish or reproduce published articles, or allow others to do so for Government purposes.     

Compounds that increase cAMP prevent ischemia-reperfusion pulmonary capillary injury.

This study evaluated the physiological effects of compounds that increase adenosine 3',5'-cyclic monophosphate (cAMP) on changes in pulmonary capillary permeability and vascular resistance induced by ischemia-reperfusion (I-R) in isolated blood-perfused rabbit lungs. cAMP was elevated by 1) beta-adrenergic stimulation with isoproterenol (ISO, 10(-5) M), 2) post-beta-receptor stimulation of adenylate cyclase with forskolin (FSK, 10(-5) M), 3) and dibutyryl cAMP (DBcAMP, 1 mM), a cAMP analogue. Vascular permeability was assessed by determining the capillary filtration coefficient (Kf,c), and capillary pressure was measured using the double occlusion technique. The total, arterial, and venous vascular resistances were calculated from measured pulmonary arterial, venous, and capillary pressures and blood flow. Reperfusion after 2 h of ischemia significantly (P less than 0.05) increased Kf,c (from 0.115 +/- 0.028 to 0.224 +/- 0.040 ml.min-1.cmH2O-1.100 g-1). These I-R-induced changes in capillary permeability were prevented when ISO, FSK, or DBcAMP was added to the perfusate at reperfusion (0.110 +/- 0.022 and 0.103 +/- 0.021, 0.123 +/- 0.029 and 0.164 +/- 0.024, and 0.153 +/- 0.030 and 0.170 +/- 0.027 ml.min-1.cmH2O-1.100 g-1, respectively). I-R significantly increased total, arterial, and venous vascular resistances. These increases in vascular resistance were also blocked by ISO, FSK, and DBcAMP. These data suggest that beta-adrenergic stimulation, post-beta-receptor activation of adenylate cyclase, and DBcAMP prevent the changes in pulmonary vascular permeability and vascular resistances caused by I-R in isolated rabbit lungs through a mechanism involving an increase in intracellular levels of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversal of increased microvascular permeability associated with ischemia-reperfusion: role of cAMP.

Ischemia-reperfusion (IR) is a form of oxidant injury known to increase microvascular permeability in the lung. Agents that increase adenosine 3',5'-cyclic monophosphate (cAMP) levels have been shown to have beneficial effects in several models of oxidant lung injury associated with increased microvascular permeability. We investigated the role of adenylate cyclase activation with isoproterenol (ISO) or forskolin (FSK) in reversing the increased microvascular permeability associated with IR. ISO or FSK administered after 45 min of ischemia and 46 min of reperfusion caused a reduction in the capillary filtration coefficient (Kfc) from 1.25 +/- 0.13 to 0.53 +/- 0.08 and 0.55 +/- 0.10 ml.min-1.cmH2O-1.100 g tissue-1, respectively, at 90 min of reperfusion. This reduction in Kfc was accompanied by a rise in perfusate cAMP levels from 16.5 +/- 4.9 and 31.2 +/- 11.9 pmol/ml at 45 min of reperfusion to 444.2 +/- 147.8 and 276.1 +/- 91.0 pmol/ml at 105 min of reperfusion in lungs treated with ISO or FSK, respectively, at 46 min of reperfusion. Dibutyryl cAMP (DBcAMP), a membrane-permeable cAMP analogue, mimicked the permeability effect by reducing Kfc to 0.67 +/- 0.15 at 90 min of reperfusion. Significant hemodynamic changes occurred but were small and cannot explain the observed effect on Kfc. Photomicrographs from lungs treated with ISO or FSK revealed a reversal of the morphological manifestations of increased microvascular permeability. We conclude that the increased microvascular permeability associated with IR can be reversed by ISO, FSK, and DBcAMP and that cAMP produced by the lung contributes to the observed reversal.     

Microcarrier-attached rat hepatocytes as a xenobiotic-metabolizing system in cocultures

A method for the primary culture of rat liver cells on collagen-coated dextran microcarriers is described. Ethoxycoumarin deethylase (EOD) activity 24 hr after inoculation was comparable for liver cells cultured on microcarriers and on collagen-coated dishes. Cells were cultured on microcarriers for up to 48 hr and retained 25% of the initial EOD-activity that was seen in freshly isolated liver cells. Microcarrier-attached hepatocytes were cocultured with BALB/c 3T3 cells to study the metabolism-mediated cytotoxicity of cyclophosphamide (CPA). In the absence of hepatocytes, growth of 3T3 cells was not affected by CPA at concentrations up to 3600 M. In coculture with hepatocytes, cytotoxicity of CPA was expressed in a time- and concentration-dependent manner. At high concentrations, CPA slightly depressed the EOD-activity of hepatocytes. Our results indicate that cocultivation of microcarrier-attached rat liver cells with target cells represents a valuable approach to the study of the metabolism-mediated toxicity of xenobiotics in vitro.Abbreviations CPA cyclophosphamide - EOD Ethoxycoumarin deethylase - FBS fetal bovine serum - HBSS Hanks' balanced salt solution - HEPES N-2-Hydroxyethylpiperazine-N-2-ethanesulfonic acid - PASA Na-pyruvate, asparagine, serine, alanine - 7-HC 7-hydroxycoumarin This work was presented in part at the VIIIth Scandinavian Workshop on In Vitro Toxicology, Kongsvoll, Norway (1990).     

Expression of syndecan, a putative low affinity fibroblast growth factor receptor, in the early mouse embryo.

Syndecan is an integral membrane proteoglycan that binds cells to several interstitial extracellular matrix components and binds to basic fibroblast-growth factor (bFGF) thus promoting bFGF association with its high-affinity receptor. We find that syndecan expression undergoes striking spatial and temporal changes during the period from the early cleavage through the late gastrula stages in the mouse embryo. Syndecan is detected initially at the 4-cell stage. Between the 4-cell and late morula stages, syndecan is present intracellularly and on the external surfaces of the blastomeres but is absent from regions of cell-cell contact. At the blastocyst stage, syndecan is first detected at cell-cell boundaries throughout the embryo and then, at the time of endoderm segregation, becomes restricted to the first site of matrix accumulation within the embryo, the interface between the primitive ectoderm and primitive endoderm. During gastrulation, syndecan is distributed uniformly on the basolateral cell surfaces of the embryonic ectoderm and definitive embryonic endoderm, but is expressed with an anteroposterior asymmetry on the surface of embryonic mesoderm cells, suggesting that it contributes to the process of mesoderm specification. In the extraembryonic region, syndecan is not detectable on most cells of the central core of the ectoplacental cone, but is strongly expressed by cells undergoing trophoblast giant cell differentiation and remains prominent on differentiated giant cells, suggesting a role in placental development. Immunoprecipitation studies indicate that the size of the syndecan core protein, although larger than that found in adult tissues (75 versus 69 x 10(3) Mr), does not change during peri-implantation development. The size distribution of the intact proteoglycan does change, however, indicating developmental alterations in its glycosaminoglycan composition. These results indicate potential roles for syndecan in epithelial organization of the embryonic ectoderm, in differential axial patterning of the embryonic mesoderm and in trophoblast giant cell function.     

Increased Survival and Differentiation of Frozen Herbaceous Plant Organ Cultures through Cold Treatment

Cold treatment of donor carnation plants (Dianthus caryophyllus L.) at 4 C for 3 days or more resulted in a doubling in the percentage of excised, frozen shoot apices which survived freezing and a 6- to 7-fold increase in the percentage which formed leaf primordia or shoots. The optimal freezing parameters for both survival and differentiation were as follows: size of the shoot apex-two to three sets of leaf primordia; dimethylsulfoxide concentration in the freezing solution-5%; time in dimethylsulfoxide prior to freezing->30 minutes; average cooling rate-≥50 C/minute; initial warming rate-about 1450 C/minute. In general, the cells in the meristematic region of the shoot apex remained viable after freezing while those in the leaf primordia did not. Viability of the meristematic cells appears to be maintained by preventing the growth of intracellular ice crystals formed during rapid cooling by rapidly passing the tissue through the temperature zone in which lethal crystal growth occurs (mechanism of Luyet). Applications of this technique are discussed.     

Decoupling of the processes of molecular oxygen synthesis and electron transport in Ca2+-depleted PSII membranes

Extraction of Ca(2+) from the O(2)-evolving complex (OEC) of photosystem II (PSII) membranes with 2 M NaCl in the light (PSII(-Ca/NaCl)) results in 90% inhibition of the O(2)-evolution reaction. However, electron transfer from the donor to acceptor side of PSII, measured as the reduction of the exogenous acceptor 2,6-dichlorophenolindophenol (DCIP) under continuous light, is inhibited by only 30%. Thus, calcium extraction from the OEC inhibits the synthesis of molecular O(2) but not the oxidation of a substrate we term X, the source of electrons for DCIP reduction. The presence of electron transfer across PSII(-Ca/NaCl) membranes was demonstrated using fluorescence induction kinetics, a method that does not require an artificial acceptor. The calcium chelator, EGTA (5 mM), when added to PSII(-Ca/NaCl) membranes, does not affect the inhibition of O(2) evolution by NaCl but does inhibit DCIP reduction up to 92% (the reason why electron transport in Ca(2+)-depleted materials has not been noticed before). Another chelator, sodium citrate (citrate/low pH method of calcium extraction), also inhibits both O(2) evolution and DCIP reduction. The role of all buffer components (including bicarbonate and sucrose) as possible sources of electrons for PSII(-Ca/NaCl) membranes was investigated, but only the absence of chloride anions strongly inhibited the rate of DCIP reduction. Substitution of other anions for chloride indicates that Cl(-) serves its well-known role as an OEC cofactor, but it is not substrate X. Multiple turnover flash experiments have shown a period of four oscillations of the fluorescence yield (both the maximum level, F(max), and the fluorescence level measured 50 s after an actinic flash in the presence of DCMU) in native PSII membranes, reflecting the normal function of the OEC, but the absence of oscillations in PSII(-Ca/NaCl) samples. Thus, PSII(-Ca/NaCl) samples do not evolve O(2) but do transfer electrons from the donor to acceptor sides and exhibit a disrupted S-state cycle. We explain these results as follows. In Ca(2+)-depleted PSII membranes, obtained without chelators, the oxidation of the OEC stops after the absorption of three quanta of light (from the S1 state), which should convert the native OEC to the S4 state. An one-electron oxidation of the water molecule bound to the Mn cluster then occurs (the second substrate water molecule is absent due to the absence of calcium), and the OEC returns to the S3 state. The appearance of a sub-cycle within the S-state cycle between S3-like and S4-like states supplies electrons (substrate X is postulated to be OH(-)), explains the absence of O(2) production, and results in the absence of a period of four oscillation of the normal functional parameters, such as the fluorescence yield or the EPR signal from S2. Chloride anions probably keep the redox potential of the Mn cluster low enough for its oxidation by Y(Z)(*).