Linkages between seagrass,mangrove and saltmarsh as fish habitat in the Botany Bay estuary,New South Wales

Shallow-water vegetated estuarine habitats, notably seagrass, mangrove and saltmarsh, are known to be important habitats for many species of small or juvenile fish in temperate Australia. However, the movement of fish between these habitats is poorly understood, and yet critical to the management of the estuarine fisheries resource. We installed a series of buoyant pop nets in adjacent stands of seagrass, mangrove and saltmarsh in order to determine how relative abundance of fishes varied through lunar cycles. Nets were released in all habitats at the peak of the monthly spring tide for 12 months, and in the seagrass habitat at the peak of the neap tide also. The assemblage of fish in each habitat differed during the spring tides. The seagrass assemblage differed between spring and neap tide, with the neap tide assemblage showing greater abundances of fish, particularly those species which visited the adjacent habitats when inundated during spring tides. The result supports the hypothesis that fish move from the seagrass to the adjacent mangrove and saltmarsh during spring tides, taking advantage of high abundances of zooplankton, and use seagrass as a refuge during lower tides. The restoration and preservation of mangrove and saltmarsh utility as fish habitat may in some situations be linked to the proximity of available seagrass.     

Dexamethasone induces irreversible G1 arrest and death of a human lymphoid cell line.

Growth of a human leukemic T-cell line (CEM C7) in 10(-6) M dexamethasone results in inhibition of growth and rapid loss of cell viability after a delay of approximately 18 to 24 hours. Analysis of dexamethasone-treated cells by flow-microfluorometry showed that they were arrested in the G1 phase of the cell cycle. Loss of cell viability began at the same time as G1 accumulation was first detectable, and 20% of all cells were found to be blocked in G1 at this time suggesting that loss of viability and G1 arrest were coincident events. Half-maximal and maximal effects on both viability and G1 arrest after 48 hours in steroid were nearly identical with respect to steroid concentration and corresponded to half-maximal and full occupancy of glucocorticoid specific receptor by hormone, consistent with a glucocorticoid receptor mediated mechanism for both phenomena. Most non-viable cells were arrested in G1, and accumulation of cells in G1 was irreversible; removal of steroid in the presence of colcemid did not result in a decreased fraction of G1 cells. Furthermore, dexamethasone treatment did not protect cells against the effects of 33258 Hoechst-amplified killing of bromodeoxyuridine substituted cells exposed to light. These results show that dexamethasone arrests these leukemic cells in G1 and strongly suggest that dexamethasone-treated cells are killed upon entry into G1.     

Enzymes of cyclic nucleotide degradation in eye tissues during experimental ocular herpes

Activity of phosphodiesterases disintegrating cAMP and cGMP in the cornea, sclera and ciliary body was investigated in health and in different stages of experimental herpetic keratitis. The problems concerning the role of the cyclase system in the pathogenesis of herpetic keratitis and the possibility of applying some of the drugs to the disease treatment are discussed.     

Interactions: Dose effect relationships and isoeffect curves

Summary Interaction from several agents, i.e., a greater or smaller effects than expected from the sum of the individual effects can be of essentially two types: a) The agents could act in paralell on the same target, and a term depending on the doses of the agents involved would have to be added to the individual dose effect relationships (parergic interaction). b) The agents could act at different points in the chain of events leading to the observed effect, and the action of the second agent, the promotor, would be, at least in part, contingent on the action of the first inducer agent so that the dose effect relationships are linked in a multiplicative manner (metergic interaction). The dose effect surfaces for interaction depend on the type of dose effect relationship of the individual agents. Formulas are given for the general cases and are exemplified in graphs. Typical isobolic diagrams are also illustrated. These formulas may be adapted to experimental data by means of non-linear regression or maximum-likelihood analysis.     

Effect of heparin on the activation of the anticoagulation system by alpha-thrombin

Heparin-regulated alpha-thrombin ability to activate the response of the anticoagulation system has been studied by the perfusion of sinocarotid area of rabbits with DIP-alpha-thrombin-heparin complex. In a series of experiments the area was perfused with 1.8 micron DIP-alpha-thrombin and significant changes in anticoagulation parameters have been registered in systemic circulation. During perfusion of sinocarotid area by DIP-alpha-thrombin-heparin complex (2 microns) no activation of anticoagulation system was noted. DIP-alpha-thrombin-heparin perfusates contained no endogenic heparin, unlike DIP-alpha-thrombin perfusates. This confirms the absence of anticoagulation system response to DIP-alpha-thrombin. Control perfusion by heparin alone in equimolar concentrations revealed no changes in anticoagulation system. It is assumed that heparin, blocking cation subcentre of the recognition centre for high molecular compounds in the enzyme molecule, prevents the response of anticoagulation system, disturbing the enzyme ability to bind to specific receptors of the vascular walls.