https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:22272 2=96% and 88% respectively). Meanwhile, statin was more effective than placebo in reducing LDL (WMD=− 0.87, 95%CI  − 1.18~ − 0.55, P<0.0001), TC (WMD=− 1.23 95%CI  − 1.35~ − 1.11, P<0.00001), TG (WMD= − 0.50, 95%CI  − 0.73~ − 0.27, P<0.00001); and statin + metformin was more effective than metformin in lowering LDL (WMD= − 0.84, 95%CI:  − 1.33~ − 0.354, P=0.0009), TC (WMD= − 1.28, 95%CI: − 1.47~ − 1.10, P<0.00001), and TG (WMD= − 0.27, 95%CI:  − 0.36~ − 0.19, P<0.00001). Heterogeneities were detected during the meta-analysis.]]> Wed 24 Jun 2020 17:48:01 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15236 Wed 11 Apr 2018 17:06:49 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15677 Wed 11 Apr 2018 15:24:49 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15981 Wed 11 Apr 2018 14:59:45 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17333 Wed 11 Apr 2018 14:41:13 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17045 Wed 11 Apr 2018 14:36:26 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13896 Wed 11 Apr 2018 14:01:17 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15696 Wed 11 Apr 2018 13:53:37 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12489 Wed 11 Apr 2018 13:13:32 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14152 Wed 11 Apr 2018 12:41:22 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15695 Wed 11 Apr 2018 12:28:11 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13200 Wed 11 Apr 2018 11:58:55 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14350 +). The effect of VTA-directed injections of SB-334867 (0 or 3 μg) on locomotor activity was also assessed. Intra-VTA, but not -PVT, SB-334867 dose-dependently attenuated S⁺-induced reinstatement (3 μg dose, p<0.01). Intra-VTA SB-334867 had no effect on locomotor activity. We conclude that OrxR1 signalling within the VTA, but not the PVT, mediates cue-induced cocaine-seeking behaviour. We hypothesize that blockade of VTA OrxR1 signalling may reduce nucleus accumbens dopamine in response to drug cue presentation.]]> Wed 11 Apr 2018 11:48:59 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13895 Wed 11 Apr 2018 11:47:28 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14417 Wed 11 Apr 2018 11:44:21 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:24259 Wed 11 Apr 2018 11:39:29 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17044 2+ and calmodulin (CaM) as regulators of the cell cycle. Ca²⁺/CaM-stimulated proteins, including the family of multifunctional Ca²⁺/CaM-stimulated protein kinases (CaMK), have also been identified as mediators of cell cycle progression. CaMKII is the best-characterized member of this family, and is regulated by multi-site phosphorylation and targeting. Using pharmacological inhibitors that were believed to be specific for CaMKII , CaMKII has been implicated in every phase of the cell cycle. However, these ‘specific’ inhibitors also produce effects on other CaMKs. These additional effects are usually ignored, and the effects of the inhibitors are normally attributed to CaMKII without further investigation. Using new specific molecular techniques, it has become clear that CaMKI is an important regulator of G₁, whereas CaMKII is essential for regulating G₂/M and the metaphase-anaphase transition. If the mechanisms controlling these events can be fully elucidated, new targets for controlling proliferative diseases may be identified.]]> Wed 11 Apr 2018 11:04:43 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14153 Wed 11 Apr 2018 10:56:29 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13893 Wed 11 Apr 2018 10:36:53 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14381 Wed 11 Apr 2018 10:04:10 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17958 Wed 11 Apr 2018 09:41:07 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13894 Wed 11 Apr 2018 09:40:23 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17101 Wed 11 Apr 2018 09:35:27 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25127 T (rs6917) polymorphism and the MTHFR 677 C>T (rs1801133) polymorphism, respectively. Results: There was no evidence of association between the PHB 1630 C>T and MTHFR 677 C>T polymorphisms with either disease for BRCA1 or BRCA2 mutation carriers when breast and ovarian cancer associations were evaluated separately. Analysis that evaluated associations for breast and ovarian cancer simultaneously showed some evidence that BRCA1 mutation carriers who had the rare homozygote genotype (TT) of the PHB 1630 C>T polymorphism were at increased risk of both breast and ovarian cancer (HR 1.50, 95%CI 1.10–2.04 and HR 2.16, 95%CI 1.24–3.76, respectively). However, there was no evidence of association under a multiplicative model for the effect of each minor allele. Conclusion: The PHB 1630TT genotype may modify breast and ovarian cancer risks in BRCA1 mutation carriers. This association need to be evaluated in larger series of BRCA1 mutation carriers.]]> Wed 07 Jul 2021 11:42:58 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17324 Tue 31 Mar 2020 08:15:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17482 Tue 16 Jun 2015 15:34:15 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14785 Sat 24 Mar 2018 08:26:30 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14330 90 different genes have been identified. In this study, we used a custom-made sequencing array based on the Affymetrix 50k platform for mutation screening in 17 known XLID genes in patients from 135 families and found eight single-nucleotide changes that were absent in controls. For four mutations affecting ATRX (p.1761M>T), PQBP1 (p.155R>X) and SLC6A8 (p.390P>L and p.477S>L), we provide evidence for a functional involvement of these changes in the aetiology of intellectual disability.]]> Sat 24 Mar 2018 08:26:21 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13923 Sat 24 Mar 2018 08:24:50 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14315 Sat 24 Mar 2018 08:24:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15635 +) or drug non-availability (S⁻). Once a stable level of responding was reached, lever pressing was extinguished. Animals were then tested for reinstatement and sacrificed immediately following the presentation of either the S⁻ or S⁺ discriminative stimuli, and Fos-protein expression was assessed in thalamic and epithalamic regions. Interestingly, significant variation was observed in reinstatement behaviour, allowing a comparison between high-reinstating (HR), low-reinstating (LR) and control animals. Compared with LR animals, HR animals exhibited increased Fos-protein expression in the PVT, intermediodorsal thalamus and the medial and lateral divisions of the habenula. Our data provide evidence that activation of thalamic and epithalamic nuclei is associated with propensity to reinstate to cocaine-seeking elicited by drug-related cues. We also build upon existing data highlighting the importance of the PVT in reinstatement behaviour.]]> Sat 24 Mar 2018 08:23:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15983 50% of asthma-related healthcare costs. New investigations into the pathogenesis of glucocorticoid resistance in severe asthma indicate that pulmonary macrophages may play central roles in promoting airway inflammation, particularly in asthma that is resistant to steroid therapy. Importantly, factors that are linked to the activation of pulmonary macrophages may contribute to glucocorticoid resistance and severe asthma. Here, we review recent advances in understanding the roles of pulmonary macrophages in the mechanisms of glucocorticoid resistance and the pathogenesis of severe asthma. We discuss the role of macrophage phenotype, infection, IFN-γ, LPS, associated signaling pathways, TNF-α, MIF, and other macrophage-associated factors. Understanding the pathogenesis of steroid-resistant severe asthma will contribute to the identification of optimal therapeutic strategies for the effective management of the disease.]]> Sat 24 Mar 2018 08:23:36 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15289 Sat 24 Mar 2018 08:21:52 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13666 Sat 24 Mar 2018 08:20:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13695 1. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals^2,3, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk⁴. Modestly powered genome-wide association studies (GWAS)^5-10 have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility¹¹. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.]]> Sat 24 Mar 2018 08:19:55 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12510 Sat 24 Mar 2018 08:18:42 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12355 Sat 24 Mar 2018 08:18:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12344 Sat 24 Mar 2018 08:18:30 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13301 Sat 24 Mar 2018 08:18:05 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12385 Sat 24 Mar 2018 08:18:01 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12386 Sat 24 Mar 2018 08:18:01 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12449 40 mV shift of the K⁺ equilibrium potential and a rise in effective K⁺ concentration (>50 mM) in the intercellular space. Together these data suggest K⁺ accumulation in the intercellular space accounts for the different responses in isolated and embedded type I hair cells. To test this notion, we exposed the preparation to hyperosmotic solutions to enlarge the intercellular space. As predicted, the K⁺ accumulation effects were reduced; however, a fit of our data with a classic diffusion model suggested K⁺ permeability, rather than the intercellular space, had been altered by the hyperosmotic change. These results support the notion that under depolarizing conditions Substantial K⁺ accumulation occurs in the space between type I hair cells and calyx. The extent of K⁺ accumulation during normal synaptic transmission, however, remains to be determined.]]> Sat 24 Mar 2018 08:17:49 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12514 Sat 24 Mar 2018 08:17:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12945 Sat 24 Mar 2018 08:17:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12549 Sat 24 Mar 2018 08:16:34 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12974 Sat 24 Mar 2018 08:16:09 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13287 Sat 24 Mar 2018 08:16:04 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13289 2 = 0.31, P = 0.001), with RR variability (r² = 0.20, P = 0.008), and with systolic blood pressure (r² = 0.16, P = 0.02). Linear regression analysis identified the former two as independent predictors of QTVN. In conclusion, elevated repolarization lability is directly associated with sympathetic cardiac activation in patients with essential hypertension.]]> Sat 24 Mar 2018 08:16:04 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13259 Sat 24 Mar 2018 08:15:59 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13276 + T cell cytokine production was abrogated. The adoptive transfer of TLR7-sufficient, but not TLR7-deficient pDC to TLR7 gene-deleted mice recapitulated the antiviral responses observed in wild-type mice and promoted virus clearance. In summary, TLR7-mediated signaling by pDC is required for appropriate innate responses to acute pneumovirus infection. It is conceivable that as-yet–unidentified defects in the TLR7 signaling pathway may be associated with elevated levels of RSV-associated morbidity and mortality among otherwise healthy human infants.]]> Sat 24 Mar 2018 08:15:16 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12415 + lymphocytes (Th2 cells) and their cytokines predominate in mild to moderate allergic asthma, whereas severe steroid-resistant asthma has more of a mixed Th2/Th1 phenotype with a Th17 component. Other immune cells, particularly neutrophils, macrophages and dendritic cells, as well structural cells such as epithelial and airway smooth muscle cells also produce disease-associated cytokines in asthma. Increased levels of these immune cells and cytokines have been identified in clinical samples and their potential role in disease demonstrated in studies using mouse models of asthma. Clinical trials with inhibitors of cytokines such as interleukin (IL)-4, -5 and tumour necrosis factor-α have had success in some studies but not others. This may reflect the design of the clinical trials, including treatments regimes and the patient population included in these studies. IL-13, -9 and granulocyte-macrophage colony-stimulating factor are currently being evaluated in clinical trials or preclinically and the outcome of these studies is eagerly awaited. Roles for IL-25, -33, thymic stromal lymphopoietin, interferon-γ, IL-17 and -27 in the regulation of asthma are just emerging, identifying new ways to treat inflammation. Careful interpretation of results from mouse studies will inform the development and application of therapeutic approaches for asthma. The most effective approaches may be combination therapies that suppress multiple cytokines and a range of redundant and disconnected pathways that separately contribute to asthma pathogenesis. Astute application of these approaches may eventually lead to the development of effective asthma therapeutics. Here we review the current state of knowledge in the field.]]> Sat 24 Mar 2018 08:14:54 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12308 Sat 24 Mar 2018 08:11:38 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:12329 Sat 24 Mar 2018 08:11:37 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17178 Sat 24 Mar 2018 08:06:32 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17046 Sat 24 Mar 2018 08:05:06 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18261 Sat 24 Mar 2018 08:04:54 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18122 2+ mobilization that leads to the contractile response to either exogenously added histamine (1 μM–1 mM) or electrical field stimulation (10 Hz, 0.5 ms, 60 V). Removal of extracellular Ca²⁺ by removal of Ca²⁺ from the bathing medium reduced histamine (1 mM) induced responses by 34% and responses induced by electrical field stimulation by 94%. Similarly, blockade of L-type Ca²⁺ channels by nifedipine (1 μM) reduced histamine (1 mM) induced responses by 43% and responses induced by electrical field stimulation by 77%. Application of cyclopiazonic acid (CPA) (10 μM) to inhibit Ca²⁺ reuptake to the sarcoplasmic reticulum enhanced both histamine-induced and electrical field stimulation induced responses to a small degree, while the addition of the inosotol triphosphate (IP3) receptor antagonist, 2-aminophenoxyethane borane (2-APB) (100 μM) inhibited histamine induced responses by 70% and electrical field stimulation induced responses by 57%. Ryanodine (1 μM) did not affect contractile responses to either histamine or electrical field stimulation, either in the absence or presence of 2-APB (100 μM). During both histamine and electrical field stimulation induced contractions, prostate smooth muscle generates IP3 receptor mediated Ca²⁺ release in conjunction with Ca²⁺ entry from the extracellular environment. Ryanodine receptors on the other hand, appear not to play a role in this physiological mechanism.]]> Sat 24 Mar 2018 08:04:47 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18166 50% of neurons within the sample. To determine whether FMISO retention occurred after the tissue was already committed to infarction, FMISO was administered 4 to 6 hours after the onset of permanent vessel occlusion. Intense FMISO retention was consistently seen throughout the infarct core. In conclusion, FMISO retention occurs both within the ischaemic penumbra and within the early infarct core. Most penumbral tissues show evidence of selective cellular injury.]]> Sat 24 Mar 2018 08:04:38 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18118 dGag_197–205 challenge compared to rDNA poxvirus prime-boost strategy. Our findings further substantiate the importance of vector selection/combination, order and route of delivery when designing effective vaccines for HIV-1.]]> Sat 24 Mar 2018 08:04:36 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18113 Sat 24 Mar 2018 08:04:36 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18116 2+-mediated activation of the anaphase-promoting complex/cyclosome (APC/C). Although the loss in activity of the M-phase kinase CDK1 is known to be an essential downstream event of this process, the contribution of phosphatases to arrest and meiotic resumption is less apparent, especially in mammals. Therefore, we explored the role of protein phosphatase 2A (PP2A) in mouse eggs using pharmacological inhibition and activation as well as a functionally dominant-negative catalytic PP2A subunit (dn-PP2Ac-L199P) coupled with live cell imaging. We observed that PP2A inhibition using okadaic acid induced events normally observed at fertilization: degradation of the APC/C substrates cyclin B1 and securin resulting from loss of the APC/C inhibitor Emi2. Although sister chromatids separated, chromatin remained condensed, and polar body extrusion was blocked as a result of a rapid spindle disruption, which could be ameliorated by non-degradable cyclin B1, suggesting that spindle integrity was affected by CDK1 loss. Similar cell cycle effects to okadaic acid were also observed using dominant-negative PP2Ac. Preincubation of eggs with the PP2A activator FTY720 could block many of the actions of okadaic acid, including Emi2, cyclin B1, and securin degradation and sister chromatid separation. Therefore, in conclusion, we used okadaic acid, dn-PP2Ac-L199P, and FTY720 on mouse eggs to demonstrate that PP2A is needed to for both continued metaphase arrest and successful exit from meiosis.]]> Sat 24 Mar 2018 08:04:35 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17481 Sat 24 Mar 2018 08:04:10 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:21473 Sat 24 Mar 2018 08:03:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17125 −10) that is also associated with risk of prostate cancer and is inversely associated with risk of type 2 diabetes.]]> Sat 24 Mar 2018 08:02:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17110 Sat 24 Mar 2018 08:02:27 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17332 Sat 24 Mar 2018 08:01:51 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17330 Sat 24 Mar 2018 08:01:51 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17343 Sat 24 Mar 2018 08:01:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17421 Sat 24 Mar 2018 08:01:37 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:16516 A receptor, and that has anti-apoptotic and anti-excitotoxic actions, reducing brain damage in adult animal models of brain injury. We sought to determine if prophylactic treatment of the pregnant female with a single dose of this steroid could reduce birth asphyxia-induced losses in hippocampal function at 5 days of age (P5) in spiny mouse neonates (Acomys cahirinus). At 37 days gestation (term = 39 days) and 1 h before inducing birth asphyxia, spiny mice dams were injected subcutaneously (0.2 ml) with either 3 mg/kg allopregnanolone or 20% w/v β-cyclodextrin vehicle. One hour later, fetuses were either delivered immediately by caesarean section (control group) or exposed to 7.5 min of in utero asphyxia, causing acidosis and hypoxia. At P5, ex vivo hippocampal plasticity was assessed, or brains collected to determine cell proliferation (proliferating cell nuclear antigen; PCNA) or calcium channel expression (inositol trisphosphate receptor type 1; IP₃R1) using immunohistochemistry. Allopregnanolone partially prevented the decrease in long term potentiation at P5, and the asphyxia-induced increase in IP₃R1 expression in CA1 pyramidal neurons. There was no effect of allopregnanolone on the asphyxia induced impairment of the input/output (I/O) curve and paired-pulse facilitation (PPF). In control birth pups, maternal allopregnanolone treatment caused significant changes in short term post-synaptic plasticity and also reduced hippocampal proliferation at P5. These findings show that allopregnanolone can modulate hippocampal development and synaptic function in a normoxic or hypoxic environment, possibly by modifying calcium metabolism. Best practice for treatment dose and timing of treatment will need to be carefully considered.]]> Sat 24 Mar 2018 08:01:15 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20387 Sat 24 Mar 2018 07:58:09 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17727 − ion conductance). Pharmacological analyses in vitro and in vivo determined that elevated Cl⁻ conductance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activity. Generation of iIL-13Tg/Il13rα1^−/−, iIL-13Tg/Il13rα2^−/−, and iIL-13Tg/Stat6^−/− mice revealed that IL-13-mediated dysregulation of epithelial architecture and Cl⁻ conductance is dependent on IL-13Rα1 and STAT-6. These observations demonstrate a central role for the IL-13/IL-13Rα1 pathway in the regulation of intestinal epithelial cell Cl⁻ secretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an important role for this pathway in secretory diarrhea.]]> Sat 24 Mar 2018 07:57:45 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17776 Sat 24 Mar 2018 07:57:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17775 A receptors, high K⁺, DA receptors) also increased or decreased cellular TH immunoreactivity but decreased or increased, respectively, the number of TH+ cells in SNc. We conclude that in adult SNc neurons: (i) TH expression is activity-dependent and begins to change ~20 h following sustained changes in neuronal activity; (ii) ion-channels and receptors mediating cell-autonomous activity or synaptic input are equally potent in altering TH expression; and (iii) activity-dependent changes in TH expression are balanced by opposing changes in the number of TH+ SNc cells.]]> Sat 24 Mar 2018 07:57:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17772 Sat 24 Mar 2018 07:57:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17737 Sat 24 Mar 2018 07:57:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17743 -/- myocytes, the propafenone enantiomers and flecainide significantly reduced arrhythmogenic Ca²⁺ waves at clinically relevant concentrations, whereas Na⁺ channel inhibitors without RyR2 blocking properties did not. In Casq2^-/- mice, 5 mg/kg R-propafenone or 20 mg/kg S-propafenone prevented exercise-induced CPVT, whereas procainamide (20 mg/kg) or lidocaine (20 mg/kg) were ineffective (n=5 to 9 mice, P<0.05). QRS duration was not significantly different, indicating a similar degree of Na⁺ channel inhibition. Clinically, propafenone (900 mg/d) prevented ICD shocks in a 22-year-old CPVT patient who had been refractory to maximal standard drug therapy and bilateral stellate ganglionectomy. RyR2 cardiac Ca²⁺ release channel inhibition appears to determine efficacy of class I drugs for the prevention of CPVT in Casq2^-/- mice. Propafenone may be an alternative to flecainide for CPVT patients symptomatic on β-blockers.]]> Sat 24 Mar 2018 07:57:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17733 C, L25P, while sequence analysis indicates both of their parents are negative for the mutation. Diagnostic restriction enzyme analysis detected low-level mosaicism of the mutation in their mother. Sister pair 2 are half-sisters who share a mother and each has the missense PCDH19 mutation c.1019 A>G, N340S. The sequence chromatograph of their mother shows reduced signal for the same mutation. These data indicate maternal somatic and gonadal mosaicism of the PCDH19 mutation in both sister pairs. Phenotyping is suggestive of, and PCDH19 mutation detection is diagnostic for, the disorder EFMR in the affected girls. Conclusions: We show that gonadal mosaicism of a PCDH19 mutation in a parent is an important molecular mechanism associated with the inheritance of EFMR. This should be considered when providing genetic counseling for couples who have one affected daughter as they may risk recurrence of affected daughters and having sons at risk of transmitting EFMR.]]> Sat 24 Mar 2018 07:57:38 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17715 Sat 24 Mar 2018 07:57:27 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17785 Sat 24 Mar 2018 07:57:23 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17759 Sat 24 Mar 2018 07:57:22 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17975 Sat 24 Mar 2018 07:56:42 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17907 1 month before their procedure into a control group (n = 18) or a fish oil group (n = 18) in an unblinded fashion. The latter were supplemented with fish oil 6 g/day for a mean of 40 ± 12 days. Pulmonary venous and left atrial effective refractory periods (ERPs), PV conduction, and susceptibility to AF initiated within PVs were assessed. Compared to the control group, the fish oil group had (1) longer left-sided (p = 0.002) and right-sided (p = 0.001) pulmonary venous ERPs; (2) less dispersion of pulmonary venous ERPs (left PVs p = 0.001, right PVs p = 0.07); (3) longer left atrial ERPs (p = 0.02); (4) no difference in pulmonary venous conduction; (5) lower incidence of AF initiated from PVs during ERP testing (77% vs 31%, p = 0.02); and (6) prolongation of mean AF cycle length (p = 0.009) and shortest AF cycle length in PVs (p = 0.04). In conclusion, patients with PAF chronically supplemented with fish oils exhibit distinctive electrophysiologic properties including prolonged pulmonary venous and left atrial ERPs and decreased susceptibility to initiation AF from within PVs. These changes may in part explain the antifibrillatory effect of chronic omega-3 polyunsaturated fatty acid supplementation in patients with PAF.]]> Sat 24 Mar 2018 07:56:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17903 Sat 24 Mar 2018 07:56:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17946 Sat 24 Mar 2018 07:56:30 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17949 Sat 24 Mar 2018 07:56:30 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17925 Sat 24 Mar 2018 07:56:24 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:19245 Sat 24 Mar 2018 07:54:57 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25275 Sat 24 Mar 2018 07:38:18 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25272 Sat 24 Mar 2018 07:38:17 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25252 Sat 24 Mar 2018 07:38:16 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25285 Sat 24 Mar 2018 07:38:12 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25110 Sat 24 Mar 2018 07:17:16 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25111 Sat 24 Mar 2018 07:17:15 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25109 Sat 24 Mar 2018 07:17:14 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:22097 Sat 24 Mar 2018 07:15:17 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25081 Sat 24 Mar 2018 07:15:04 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:22547 Sat 24 Mar 2018 07:14:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17322 Mon 06 Apr 2020 12:14:32 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27736 Fri 26 May 2017 11:27:53 AEST ]]>