https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 Polarized and persistent Ca²⁺ plumes define loci for formation of wall ingrowth papillae in transfer cells https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26914 cyt) of cells trans-differentiating to a transfer cell morphology was tested. This hypothesis was examined using Vicia faba cotyledons. On transferring cotyledons to culture, their adaxial epidermal cells synchronously trans-differentiate to epidermal transfer cells. A polarized and persistent Ca²⁺ signal, generated during epidermal cell trans-differentiation, was found to co-localize with the site of ingrowth wall formation. Dampening Ca²⁺ signal intensity, by withdrawing extracellular Ca²⁺ or blocking Ca²⁺ channel activity, inhibited formation of wall ingrowth papillae. Maintenance of Ca²⁺ signal polarity and persistence depended upon a rapid turnover (minutes) of cytosolic Ca²⁺ by co-operative functioning of plasma membrane Ca²⁺-permeable channels and Ca²⁺-ATPases. Viewed paradermally, and proximal to the cytosol-plasma membrane interface, the Ca²⁺ signal was organized into discrete patches that aligned spatially with clusters of Ca²⁺-permeable channels. Mathematical modelling demonstrated that these patches of cytosolic Ca²⁺ were consistent with inward-directed plumes of elevated [Ca²⁺]cyt. Plume formation depended upon an alternating distribution of Ca²⁺-permeable channels and Ca²⁺-ATPase clusters. On further inward diffusion, the Ca²⁺ plumes coalesced into a uniform Ca²⁺ signal. Blocking or dispersing the Ca²⁺ plumes inhibited deposition of wall ingrowth papillae, while uniform wall formation remained unaltered. A working model envisages that cytosolic Ca²⁺ plumes define the loci at which wall ingrowth papillae are deposited.]]> Wed 11 Apr 2018 16:31:50 AEST ]]> A theoretical model of slow wave regulation using voltage-dependent synthesis of inositol 1,4,5-trisphosphate https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1395 Wed 11 Apr 2018 15:40:46 AEST ]]> A theoretical model of slow wave regulation using voltage-dependent synthesis of inositol 1,4,5-trisphosphate https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:3114 Wed 11 Apr 2018 14:34:07 AEST ]]> Pharmacological approaches that slow lymphatic flow as a snakebite first aid https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14540 Wed 11 Apr 2018 10:55:00 AEST ]]> Color enhancement in endoscopic images using adaptive sigmoid function and space variant color reproduction https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:28085 Wed 11 Apr 2018 10:23:54 AEST ]]> Role of voltage-dependent modulation of store Ca2+ release in synchronization of Ca2+ oscillations https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1132 Wed 11 Apr 2018 09:44:22 AEST ]]> Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:16993 450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.]]> Wed 11 Apr 2018 09:23:28 AEST ]]> Ketamine anesthesia helps preserve neuronal viability https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:9604 Sat 24 Mar 2018 08:39:39 AEDT ]]> Generation and propagation of gastric slow waves https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:9515 Sat 24 Mar 2018 08:35:35 AEDT ]]> Ca²⁺ phase waves: a basis for cellular pacemaking and long-range synchronicity in the guinea-pig gastric pylorus https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1733 Sat 24 Mar 2018 08:27:27 AEDT ]]> SR Ca²⁺ store refill-a key factor in cardiac pacemaking https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:9917 Sat 24 Mar 2018 08:13:33 AEDT ]]> Synchronization of Ca²⁺ oscillations: a coupled oscillator-based mechanism in smooth muscle https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:10403 Sat 24 Mar 2018 08:07:46 AEDT ]]> Electrophysiological properties of rat mesenteric lymphatic vessels and their regulation by stretch https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20078 Sat 24 Mar 2018 08:00:08 AEDT ]]> Differences in the regulation of RyR2 from human, sheep, and rat by Ca²⁺ and Mg²⁺ in the cytoplasm and in the lumen of the sarcoplasmic reticulum https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18980 i = 10 µM at 100 nM Ca²⁺) that was similar to RyR2 from rat and sheep obtained under the same experimental conditions. However, in the presence of 0.1 mM Ca²⁺, RyR2s from human were 3.5-fold less sensitive to cytoplasmic Mg²⁺ inhibition than those from sheep and rat. The Kₐ values for luminal Ca²⁺ activation were similar in the three species (35 µM for human, 12 µM for sheep, and 10 µM for rat). From the relationship between open probability and luminal [Ca²⁺], the peak open probability for the human RyR2 was approximately the same as that for sheep, and both were ~10-fold greater than that for rat RyR2. Human RyR2 also showed the same sensitivity to luminal Mg²⁺ as that from sheep, whereas rat RyR2 was 10-fold more sensitive. In all species, modulation of RyR2 gating by luminal Ca²⁺ and Mg²⁺ only occurred when cytoplasmic [Ca²⁺] was <3 µM. The activation response of RyR2 to luminal and cytoplasmic Ca²⁺ was strongly dependent on the Mg²⁺ concentration. Addition of physiological levels (1 mM) of Mg²⁺ raised the Kₐ for cytoplasmic Ca²⁺ to 30 µM (human and sheep) or 90 µM (rat) and raised the Kₐ for luminal Ca²⁺ to ~1 mM in all species. This is the first report of the regulation by Ca²⁺ and Mg²⁺ of native RyR2 receptor activity from healthy human hearts.]]> Sat 24 Mar 2018 07:58:52 AEDT ]]> Spontaneous transient depolarizations in lymphatic vessels of the guinea pig mesentery: pharmacology and implication for spontaneous contractility https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:4460 Sat 24 Mar 2018 07:18:30 AEDT ]]> Essential role of calmodulin in RyR inhibition by dantrolene https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:22802 2+ release. Although dantrolene inhibits Ca2+ release from the sarcoplasmic reticulum of skeletal and cardiac muscle preparations, its mechanism of action has remained controversial, because dantrolene does not inhibit single ryanodine receptor (RyR) Ca2+ release channels in lipid bilayers. Here we test the hypothesis that calmodulin (CaM), a physiologic RyR binding partner that is lost during incorporation into lipid bilayers, is required for dantrolene inhibition of RyR channels. In single channel recordings (100 nM cytoplasmic [Ca2+] + 2 mM ATP), dantrolene caused inhibition of RyR1 (rabbit skeletal muscle) and RyR2 (sheep) with a maximal inhibition of Po (Emax) to 52 ± 4% of control only after adding physiologic [CaM] = 100 nM. Dantrolene inhibited RyR2 with an IC50 of 0.16 ± 0.03 µM. Mutant N98S-CaM facilitated dantrolene inhibition with an IC50 = 5.9 ± 0.3 nM. In mouse cardiomyocytes, dantrolene had no effect on cardiac Ca2+ release in the absence of CaM, but reduced Ca2+ wave frequency (IC50 = 0.42 ± 0.18 µM, Emax = 47 ± 4%) and amplitude (IC50 = 0.19 ± 0.04 µM, Emax = 66 ± 4%) in the presence of 100 nM CaM. We conclude that CaM is essential for dantrolene inhibition of RyR1 and RyR2. Its absence explains why dantrolene inhibition of single RyR channels has not been previously observed.]]> Sat 24 Mar 2018 07:12:18 AEDT ]]> Beta-adrenergic stimulation increases RyR2 activity via intracellular Ca²⁺ and Mg²⁺ regulation https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13304 a and maximum levels of cytoplasmic Ca²⁺ activation site were not affected by ß-adrenergic stimulation. Our RyR2 gating model was fitted to the single channel data. It predicted that in diastole, ß-adrenergic stimulation is mediated by 1) increasing the activating potency of Ca²⁺ binding to the luminal Ca²⁺ site and decreasing its affinity for luminal Mg²⁺ and 2) decreasing affinity of the low-affinity Ca²⁺/Mg²⁺ cytoplasmic inhibition site. However in systole, ß-adrenergic stimulation is mediated mainly by the latter.]]> Mon 24 Sep 2018 13:24:28 AEST ]]>