Ixodes tasmani is one of the most common and widespread of the Australian species of Ixodes and a vector of zoonotic rickettsial diseases. The tick was reared successfully in the laboratory; the entire life cycle was completed in 4 months. A diurnal rhythm of detachment from captive hosts (laboratory Rattus norvegicus) was observed for all stages and, combined with other evidence, suggests that I. tasmani is nidicolous. The prevalence and intensity of tick infestation on wild-caught, common brushtail possums (Trichosurus vulpecula), was least during the summer months. To investigate questing activity, laboratory-reared nymphs were held in enclosures in one sheltered (tree hollows) and three exposed (vegetation) microhabitats. Questing was continuous but at low intensity in tree hollows, and nocturnal and at an increased (higher) intensity in vegetation. The observed questing activity appeared to maximise host contact with T. vulpecula, which is nocturnal but retires by day to tree hollows. Field and laboratory observations suggest that the risk for humans of tick-bite from I. tasmani and consequent transmission of zoonotic diseases may be low compared with the risk from other tick species.
Treatment of intact human platelets with the tumour-promoting phorbol ester, phorbol 12-myristate 13-acetate (PMA), specifically inhibited PGD2-induced cyclic AMP formation without affecting the regulation of cyclic AMP metabolism by PGL z, PGE 1, 6-keto-PGEl, adenosine or adrenaline. This action of PMA was: (i) concentration-dependent; (ii) not mediated by evoked formation or release of endogenous regulators of adenylate cyclase activity (thromboxane A 2 or ADP); (iii) mimicked by 1,2-dioctanoylglycerol (DiCs) but not by 4~t-phorbol 12,13-didecanoate (which does not activate protein kinase C); (iv) attenuated by Staurosporine. These results indicate that activation of protein kinase C in platelets may provide a regulatory mechanism to abrogate the effects of the endogenous adenylate cyclase stimulant PGD 2 without compromising the effects of exogenous stimulants of adenylate cyclase (PGI 2, 6-keto-PGE1, adenosine).
Exogenous synthetic 1,2-diacylglycerols (e.g. 1,2-dioctanoylglycerol, DiC8) and 4β Phorbol esters (e.g. phorbol myristate acetate, PMA) routinely are used to probe the effects of protein Kinase C (PKC) on cellular responsiveness. Such agents act either independently or synergistically with elevated [Ca2+]i to induce platelet activation, but also inhibit agonist-induced inositol lipid metabolism and Ca2+ flux. These findings led to the concept that activated PKC can function as a bi-directional regulator of platelet reactivity. Therefore, DiCg and PMA were utilized to examine the effects of activated PKC on receptor-mediated stimulation and inhibition of adenylate cyclase, as monitored by cAMP accumulation. All studies were performed using intact human platelets in a modified Tyrodes solution, and cAMP was quantified by radioimmunoassay. Pretreatment (2 min.; 37°C) of platelets with PMA (≤ 300 nM) but not DiCg (200 μM) attenuated the elevation of platelet cAMP content evoked by PGD2 300 nM) but not by PGE1 (≤300 nM), PGI2 (≤100 nM) or adenosine (≤ 100 μM).These effects of PMA were unaffected by ADP scavengers, by Flurbiprofen (10 μM) or by cAMP phosphodiesterase inhibitors (IBMX, 1 mM) but were abolished by the PKC inhibitor Staurosporine (STP, 100 nM). In contrast, DiC8 (200 μM), but not PMA ( ≤ 300 nM), reduced the inhibitory effect of adrenaline (5 μM) on PGE1 (300 nM)-induced cAMP formation. This effect of DiCg was unaltered by STP (100 nM). Selective inhibition of PGD2-induced cAMP formation by PMA most probably can be attributed to PKC catalysed phosphorylation of the DP receptor. Reduction of the inhibitory effect of adrenaline by DiC8 could occur via an action at the α2 adrenoreceptor or Ni. These differential effects of PMA and DiC8 may result from differences in their distribution or efficacy, or to heterogeneity of platelet PKC.
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