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The former and current distribution of the quokka, Setortix brachyurus, was mapped from published and all available unpublished records. At the time of European settlement the quokka was widespread and abundant and its distribution encompassed an area of approximatelyThe former and current distribution of the quokka, Setortix brachyurus, was mapped from published and all available unpublished records. At the time of European settlement the quokka was widespread and abundant and its distribution encompassed an area of approximately 41 200 km2 of south-west Western Australia inclusive of two offshore islands, Bald Island and Rottnest Island. Historical reports indicated an extensive population decline occurred in the 1930s. The decline continued, with a previously undocumented decline apparent in the period from 1980 to 1992. However, this decline may be an artefact of the time scales used for mapping and may well equate with a previously reported decline lor a suite of south -west mammals in the 1970s. By 1992 the quokka´s distribution had been reduced to an area of approximately 17800 km2. An increased awareness of the presence of the quokka on the mainland has resulted in numerous reportings of quokka presence since 1992, has confimled the existence of several populations at the northern extent of the quokka´´s known geographic range and indicated the cmrent, 2005, distribution to be similar to that in 1992. However, survey and population estimates at six of these mainland locations from the northem jarrah forest indicated low abundance. There have been no population estimates elsewhere on the mainland. Two populations have been reported tiom the Swan Coastal Plain, but neither has been confirmed extant. Predation by the introduced fox, Vulpes vulpes, is implicated as a major cause of the quokka´s initial decline, while ongoing predation, habitat destruction and modification through altered tire regimes have contributed to the continued decline. Specific conservation management actions are recommended, namely: (i) Implementing an active adaptive management program in the northern jarrah forest to determine quokka population response to habitat manipulation through the use of fIre, fox baiting and pig control; (ii) Surveying the Stirling fumge and Green Range populations with emphasis placed on determining population size and population genetic structure; (iii) Surveying the reported occurrences from the Swan Coastal Plain, with emphasis on unambiguously determining presence. If confirmed, priority should he directed to assessing population size and determining the management requirements to ensure persistence of the population; (iv) Surveying southem forest and south coast populations to assess quokka population size, the extent of movement between sllbpopulations and assessment of the range of habitat types used by quokkas. The latter should be combined with spatial analyses of known extant populations and suitable and potentially suitable habitat; (v) Determining the role of tire in establishing and maintaining preferred habitat of southern forest and south coast populations; and (vi) Establishing a program to assess the potential effects from management operations.
Total body water increases in pregnancy and while the uterus, placenta, fetus, and amniotic fluid constitute part of this increase, the largest component is in the extracellular water. Fat stores also increase and thus the distribution volumes of all drugs expand, but the major effect is seen in polar drugs which are confined to the extracellular space. Cardiac output and renal function also increase and elimination of polar drugs is acelerated. In contrast, the elimination of lipophilic drugs may be retarded, and the effect on intermediate drugs is variable. Polar drugs cross the placenta slowly and accumulate in amniotic fluid and therefore in the fetal gut lumen. Lipophilic drugs cross the placenta rapidly and their transplacental distribution is dependent on relative maternal and fetal affinity: this is determined largely by protein binding on either side of the placenta. The. fetus and neonate dispose of all drugs less rapidly than adults, the most efficient elimination processes being sulphate conjugation and renal excretion.
A skeletal world revision of the genus is presented to accompany a family account for Flora Malesiana. 82 species are recognised, of which 74 occur in the Malesiana region. Six species are desctibed as new, one species is raised from infraspecific status, and five species are restored from synonymy. Many names are typified for the first time. Three widespread, or locally abundant hybrids are also included. Full descriptions are given for new (6) or recircumscribed (7) species, and emended descriptions of species arc given where necessary (9). Critical notes are given for all the species. Little known and excluded species are discussed. An index to all published species names and an index of exsiccatae is given.
Through the kind assistance of O. G. Lloyd of Cincinnati, Ohio, most of the Australian polypores in our possession have been accurately identified. In the present paper we record our various collections. In doing so, we make use of the excellent keys employed by Lloyd in the following works: "Synopsis of the Genus Hexagona" (Ohio, 1910), "Synopsis of the Stipitate PoIyporoids" (Ohio, 1912), "Synopsis of the Section Apus of the Genus Polyporus" (Ohio, 1915) and "Synopsis of the Genus Fomes" (Ohio, 1915). In addition to recording the plants we have handled, we have included as well all the Australian species embraced in these works. Australian mycologists should thus have available a workable scheme for the identification of most of our firmer polypores. Those who have attempted to work out the species from Cooke´s "Handbook of Australian Fungi", will appreciate the value of Lloyd´s work. We deal first with the Stipitate Polypores, then with Fomes, Polyporus (Apus) and Hexagona.
In this thesis I have investigated the regulation of eicosanoid synthesizing-enzymes by cannabinoid receptor agonists. Rat renal mesangial cells were used as a model system. I could show that all three (CB1, CB2, and GPR55) cannabinoid receptors are expressed on the mRNA level in rat renal mesangial cells – but with differing expression profiles. The CB1 and GPR55 receptors are expressed in comparable amounts, whereas the CB2 receptor is considerably less expressed than the CB1 and the GPR55 receptors. Furthermore I could show that stimulation of renal mesangial cells with CB1 receptor agonists, such as R(+)MA or ACEA, increased IL-1β-induced cPLA2, sPLA2-IIa, and COX2 protein and mRNA expression which subsequently led to an enhanced IL-1β-induced PGE2 formation. Additionally, the IL-1β- induced sPLA2-IIa promoter activity was also increased by CB1 receptor stimulation. Besides the modulated expression of the eicosanoid synthesizing enzymes, I could show that CB1 agonists also led to an increase of IL-1β-induced iNOS expression and subsequent NO formation. In contrast, stimulation with CB2 selective agonists led to a decrease in IL-1β- induced sPLA2-IIa protein expression and PGE2 formation. Accordingly, the IL-1β-induced sPLA2-IIa promoter activity was also reduced by CB2 receptor agonists. IL-1β-induced iNOS expression and subsequent NO formation were not influenced by CB2 recptor activation. Matching the results I obtained with CB1 receptor agonists on IL-1β-induced PGE2 formation, I could observe an increased cPLA2 protein and mRNA expression with a subsequent increase in IL-1β-induced PGE2 formation by GPR55 stimulation. Stimulation with THC, an unselective CB agonist, increased the IL-1β-induced sPLA2-IIa protein expression and subsequently led to an enhanced IL-1β-induced PGE2 formation. Subjecting the cells to higher THC concentrations surprisingly led to a reduction of the IL-1b-induced sPLA2-IIa protein expression and PGE2 formation. A possible explanation may be the differential expression of the three CB receptors. At low concentrations THC may predominantly activate CB1 and GPR55 and with increasing concentration CB2 receptors may also be activated, slightly reversing the enhancing effect. Moreover, I could show that the CB1 receptor stimulation mediated phosphorylation and hence the activation of ERK1/2 MAPK. Additionally to ERK1/2, there was also a phosphorylation and activation of NFkB observed by CB1 receptor stimulation. In my thesis I could show for the first time that PPARα was activated by IL-1β in rMC. The IL-1β-induced PPARα promoter activity was completely inhibited by addition of the CB2 receptor agonist, JWH015. These findings were confirmed by inhibition of the IL-1β-induced PGE2 formation by a PPARα antagonist (MK-886). In summary, I could show that activation of CB1 receptors in our system led to a worsening of an inflammatory condition, whereas activation of the CB2 receptors led to the complete opposite; namely a reduction of the inflammatory response by reducing the sPLA2-IIa expression and PGE2 formation. GPR55 activation did not display any alteration of inflammatory conditions, since the classical inflammatory pathway was not influenced.