Peat and water chemistry at Big Run Bog,a peatland in the Appalachian mountains of West Virginia,USA

At Big Run Bog, aSphagnum-dominated peatland in the unglaciated Appalachian Plateau of West Virginia, significant spatial variation in the physical and chemical properties of the peat and in surface and subsurface (30 cm deep) water chemistry was characterized. The top 40 cm of organic peat at Big Run Bog had average values for bulk density of 0.09 g · cm^–3, organic matter concentration of 77%, and volumetric water content of 88%. Changes in physical and chemical properties within the peat column as a function of depth contributed to different patterns of seasonal variation in the chemistry of surface and subsurface waters. Seasonal variation in water chemistry was related to temporal changes in plant uptake, organic matter decomposition and element mineralization, and to varying redox conditions associated with fluctuating water table levels. On the average, total Ca, Mg, and N concentrations in Big Run Bog peat were 33, 15, and 1050 mol · g^–1, respectively; exchangeable Ca and Mg concentrations were 45 and 14 eq · g^–1 , respectively. Surface water pH averaged 4.0 and Ca⁺⁺ concentrations were less than 50 eq · L^–1 . These chemical variables have all been used to distinguish bogs from fens. Physiographically, Big Run Bog is a minerotrophic fen because it receives inputs of water from the surrounding forested upland areas of its watershed. However, chemically, Big Run Bog is more similar to true ombrotrophic bogs than to minerotrophic fens.     

High diversity and low specificity of fungi associated with seedless epiphytic plants

Epiphytes, which grow on other plants for support, make up a large portion of Earth's plant diversity. Like other plants, their surfaces and interiors are colonized by diverse assemblages of fungi that can benefit their hosts by increasing tolerance for abiotic stressors and resistance to disease or harm them as pathogens. Fungal communities associated with epiphytic plants and the processes that structure these communities are poorly known. To address this, we sampled seven epiphytic seedless plant taxa in a Costa Rican rainforest and examined the effects of host identity and microhabitat on external and endophytic fungal communities. We found low host specificity for both external and endophytic fungi and weak differentiation between epiphytic and neighboring epilithic plant hosts. High turnover in fungi within and between hosts and habitats reveals that epiphytic plant-associated fungal communities are highly diverse and suggests that they are structured by stochastic processes.     

Classification of non-Hodgkin's lymphomas: facts and perspectives]

Previous classifications of malignant non-Hodgkin lymphomas (nHL) are based on morphological and histological-cytological findings. The rapid development of immunology, the application of immunocytological, cytochemical and electromicroscopic methods led to new classifications of nHL based on immunology. They are founded on the idea that the prevailing cells of nHL correspond to a cell type from the differentiation line of lymphocytes. Thus, a distinction can be made between malignant lymphomas (ml) of stem, B and T-cells; the more frequently occurring lymphomas originating from B-cells are represented by chronic lymphatic leukaemia originating from B1-cells, by ml of follicular genesis (centrocytes, centroblastic-centrocytic ml, centroblasts) and by ml synthesizing and releasing immunoglobulins (immunocytoma, immunoblastoma). The type formerly called "reticulosarcoma" (histocytic ml) could be identified to be an immature, Ig synthesizing ml (immunoblastloma) in most cases. The new classification enables a more extensive differentiation and a better prognostic statement to be made than previous ones. The new units of disease can be diagnosed in most cases with light microscopic routine methods, although borderline cases and unclassifiable ml may occur.     

Hexadecylphosphocholine inhibits translocation of CTP:choline-phosphate cytidylyltransferase in Madin-Darby canine kidney cells.

The mechanism of the inhibition of phosphatidylcholine biosynthesis by the phospholipid analogue, hexadecylphosphocholine, was investigated in Madin-Darby canine kidney cells. In the presence of 50 mumol/liter hexadecylphosphocholine, there was a translocation of CTP:choline-phosphate cytidylyltransferase (EC 22.7.7.15) activity from the membranes to the cytosol of the cells. Since we recently demonstrated that hexadecylphosphocholine also inhibits protein kinase C in vitro, [methyl-3H]choline labeling experiments were repeated with phorbol ester-desensitized cells. In these cells the same inhibitory effect of hexadecylphosphocholine was measured. As a consequence of inhibition, the [methyl-3H]choline incorporation into the phosphocholine pool was increased time-dependently. In addition, there was no evidence for a difference between the choline uptake of control and hexadecylphosphocholine-treated cells. Likewise, the amount of diacylglycerol, a known activator of the translocation process, was not reduced. Finally, we showed that the inhibitory effect of hexadecylphosphocholine on CTP:choline-phosphate cytidylyltransferase translocation cannot be explained by the detergent properties of this phospholipid analogue. Therefore, we suggest a direct inhibitory effect of hexadecylphosphocholine on the translocation of CTP:choline-phosphate cytidylyltransferase.     

Cell volume and the regulation of apoptotic cell death

Apoptosis is a physiological mechanism allowing for the removal of abundant or potentially harmful cells. The hallmarks of apoptosis include degradation of cellular DNA, exposure of phosphatidylserine at the outer leaflet of the cell membrane and cell shrinkage. Phosphatidylserine exposure favours adhesion to macrophages with subsequent phagocytosis of the shrunken apoptotic particles. The interaction of cell volume regulatory mechanisms and apoptosis is illustrated in two different model systems, i.e. (a) lymphocyte apoptosis following stimulation of CD95 receptor and (b) erythrocyte apoptosis upon cell shrinkage. (a) Triggering of CD95 in Jurkat T lymphocytes is paralleled by activation of cell volume regulatory Cl- channels, inhibition of the Na+/H+ exchanger and osmolyte release. The latter coincides with cell shrinkage, DNA fragmentation and phosphatidylserine exposure. CD95 stimulation leads to early inhibition of the voltage gated K+ channel Kv1.3, which may contribute to the inhibition of the Ca2+ release activated Ca2+ channel I(CRAC). (b) Osmotic shock of erythrocytes activates a cell volume regulatory cation conductance allowing the entry not only of Na+ but of Ca2+ as well. Increased cytosolic Ca2+ stimulates a scramblase which disrupts the phosphatidylserine asymmetry of the cell membrane, leading to phosphatidylserine exposure. The cation conductance is further activated by oxidative stress and energy depletion and inhibited by Cl-. Shrinkage of erythrocytes stimulates in addition a sphingomyelinase with subsequent formation of ceramide which potentiates the effect of cytosolic Ca2+ on phosphatidylserine. In conclusion, cell volume-sensitive mechanisms participate in the triggering of apoptosis following receptor stimulation or cell injury.     

Effect of Vibrio parahaemolyticus haemolysin on human erythrocytes

Haemolysin Kanagawa, a toxin from Vibrio parahaemolyticus, is known to trigger haemolysis. Flux studies indicated that haemolysin forms a cation channel. In the present study, channel properties were elucidated by patch clamp and functional significance of ion fluxes by fluorescence-activated cell sorting (FACS) analysis. Treatment of human erythrocytes with 1 U ml-1 haemolysin within minutes induces a non-selective cation permeability. Moreover, haemolysin activates clotrimazole-sensitive K+ channels, pointing to stimulation of Ca2+-sensitive Gardos channels. Haemolysin (1 U ml-1) leads within 5 min to slight cell shrinkage, which is reversed in Ca2+-free saline. Erythrocytes treated with haemolysin (0.1 U ml-1) do not undergo significant haemolysis within the first 60 min. Replacement of extracellular Na+ with NMDG+ leads to slight cell shrinkage, which is potentiated by 0.1 U ml-1 haemolysin. According to annexin binding, treatment of erythrocytes with 0.1 U ml-1 haemolysin leads within 30 min to breakdown of phosphatidylserine asymmetry of the cell membrane, a typical feature of erythrocyte apoptosis. The annexin binding is significantly blunted at increased extracellular K+ concentrations and by K+ channel blocker clotrimazole. In conclusion, haemolysin Kanagawa induces cation permeability and activates endogenous Gardos K+ channels. Consequences include breakdown of phosphatidylserine asymmetry, which depends at least partially on cellular loss of K+.