https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54124 Wed 28 Feb 2024 15:15:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45084 Wed 26 Oct 2022 14:04:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48905 Wed 19 Apr 2023 16:25:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34568 Wed 17 Nov 2021 16:28:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27369 13), associated with low fibrinogen [median,<0.01g/L;IQR:<0.01-0.9g/L), low factor V levels [median,<5%;IQR:<5-4%], low factor VIII levels [median,40%;IQR:12-79%] and low factor X levels [median,48%; IQR:29-67%]. There were smaller reductions in factors II, IX and VII over time. All factors recovered over 48h post-antivenom. The median INR remained >3 at 6h post-antivenom but had reduced to <2, by 24h. The aPTT had also returned to close to normal (<50sec) at 24h. Factor VII, VIII and IX levels were unusually high pre-antivenom, median peak concentrations of 393%, 307% and 468% respectively. Pre-antivenom venom concentrations and the INR (r=0.20, p=0.02) and aPTT (r=0.19, p=0.03) were correlated (non-parametric Spearman analysis). Conclusions: Russell's viper coagulopathy results in prolonged aPTT, INR, low fibrinogen, factors V, VIII and X which recover over 48h. Severity of clotting abnormalities was associated with venom concentrations.]]> Wed 11 Apr 2018 11:40:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19519 Wed 11 Apr 2018 09:27:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49273 Wed 10 May 2023 12:10:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55100 Wed 10 Apr 2024 08:45:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33107 Wed 04 Sep 2019 09:55:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38373 80% of 18 samples as having short, medium or long telomeres compared with 33–72% using other methods.]]> Wed 01 Sep 2021 12:47:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36679 Thrombosis Research, Vol. 179, p. 28-30.]]> Tue 23 Jun 2020 15:03:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37665 2 ≥ 0.997). However, TruCount beads produced the most consistent (concentration variation = 3.8%) calculated numbers of plasma CD41⁺/Annexin V⁺ MV, which were significantly higher from that calculated using either Flow-Count or CountBright (p < 0.001). The FACSCanto was able to resolve 0.5 μm beads by FSC and 0.16 μm beads by SSC, but there were significantly more background events using SSC compared with FSC (3113 vs. 470; p = 0.008). In general, sample analysis by SSC resulted in significantly higher numbers of MV (p < 0.0001) but was well correlated with enumeration by FSC for all MV subtypes (ρ = 0.62–0.89, p < 0.0001). We conclude that all counting beads provided linear results at concentrations ranging from 6 beads/μl to 100 beads/μl, but TruCount was the most consistent. Using SSC to gate MV events produced high background which negatively affected counting bead enumeration and overall MV calculations. Strategies to reduce SSC background should be employed in order to reliably use this technique.]]> Tue 09 Mar 2021 18:12:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42910 Tue 06 Sep 2022 15:49:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34451 Tue 03 Sep 2019 18:26:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34397 in vitro. Notably, only the first eluted MP fraction bound HK₂ cells indicating a possible association between MP size and cell‑targeting properties.]]> Tue 03 Sep 2019 18:26:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14861 Thu 28 Aug 2014 12:16:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50528 Thu 27 Jul 2023 15:58:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50338 .8) for most normal cell types and did not require any manual reassignment. The AI digital differential was less reliable for abnormal blood films (r = .50-.87), but could be greatly improved by manual assessment of digital images for most cell types (r > .95) with the exception of immature granulocytes (r = .62). For blast identification, initial AI digital differentials showed 96% sensitivity and 25% specificity, which was improved to 99% and 84%, respectively, after manual digital review.Conclusions: The Techcyte platform allowed remote viewing and manual analysis of digitized slides that was comparable to microscopy. The AI software produced adequate WBC differentials for normal films and had high sensitivity for blast identification in malignant films.]]> Thu 20 Jul 2023 11:18:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26559 Thu 17 Feb 2022 09:28:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31275 Thu 13 Jan 2022 10:30:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13951 Sat 24 Mar 2018 10:41:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9688 Sat 24 Mar 2018 08:39:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8029 Sat 24 Mar 2018 08:36:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7335 Sat 24 Mar 2018 08:35:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13913 C) and rs5275 (T > C) polymorphisms was performed by real-time polymerase chain reaction using allele-specific probes. Results: Ingestion of any NSAID in the week prior to interview was associated with an elevated risk for ACS: adjusted odds ratio 1.8 (1.2, 2.5). The rs 20417 and rs 5275 polymorphisms were not singly associated with risk for ACS: adjusted odds ratios 1.1 (0.80, 1.5) and 1.2 (0.88, 1.5), respectively. Individually, the polymorphisms did not modify the risk of ACS with the drugs. When analyses were conducted by haplotype, the adjusted odds ratio with celecoxib or rofecoxib in individuals who had one or two copies of the ‘low risk’ haplotype (no GT) was 1.2 (0.29, 5.0), compared with 2.1 (1.1, 4.0) with the ‘high risk’ haplotype (one or two copies of GT). Conclusions: We found little evidence of a gene/drug interaction. We found a statistically non-significant trend toward a lower risk of coronary events with NSAIDs in the presence of the ‘low risk’ haplotype. Even if confirmed, the clinical utility of the finding would be limited as this haplotype is carried by a minority of the population.]]> Sat 24 Mar 2018 08:25:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10024 Sat 24 Mar 2018 08:12:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20929 n=41) and female (n=53). Platelet coagulation parameters including factors I, II, V, VII, VIII, IX, X, vWF:Ag and endogenous thrombin potential were measured at baseline and 4 weeks post supplementation with EPA-rich or DHA-rich oil capsules. Results: We have previously reported that platelet aggregation is specifically reduced by supplementation with EPA in males and DHA in females. This sex-specific effect was also observed for decreases in plasma levels of Factor II (-7.9±3.8%, P=.026), Factor V (-6.5±4.5%, P=.022) and vWF:Ag (-7.3±2.1%, P=.034) and was most pronounced in males supplemented with EPA. In contrast, DHA-mediated reduction in platelet aggregation in females was not accompanied by any significant changes in the coagulation parameters tested. Conclusion: Significant interactions between sex and specific LCn-3PUFA exist to reduce procoagulant activity differentially in males vs. females and could have profound effects on managing risk of thrombotic disease.]]> Sat 24 Mar 2018 08:06:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20732 Sat 24 Mar 2018 08:00:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18969 Sat 24 Mar 2018 07:58:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19564 Sat 24 Mar 2018 07:58:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20117 Sat 24 Mar 2018 07:51:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5432 Sat 24 Mar 2018 07:48:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5366 Sat 24 Mar 2018 07:43:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27930 s, was -0.34 and -0.30 respectively, p<0.05) and positively correlated with the ELISA MP-activity assay (r_s=0.42 for both, p<0.05). In addition, endothelial MV levels weakly correlated with white cell counts (r_s = 0.27, p<0.05). Conclusions Thrombin generation and flow cytometry for phosphatidylserine or tissue factor expressing MV correlate well as markers for procoagulant activity. A combination of optical or non-optical enumeration as well as functional methods may be required for a complete profiling of circulating MV.]]> Sat 24 Mar 2018 07:36:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30301 0.05). The inconsistency between results reported in the present study and other studies may be unique to the study population or be a result of the lack of a reliable standardized method for determining absolute sCD36 concentrations. However, further investigations are required to assess CD36 tissue expression in the study population and to assess the accuracy of various commercially available sCD36 ELISA kits. Thus, the availability of a standardized simple sCD36 ELISA that could be performed in any basic laboratory would be more favorable to the specialized flow cytometry methods that detect CD36⁺ microparticles if it was to be used as a biomarker.]]> Sat 24 Mar 2018 07:31:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27245 g=0.96, SE=0.47, P=9x10⁻⁴) and profile scores (r_g=0.72; 95% confidence interval, 0.52–0.93). Between LAA and cardioembolism and SVD and cardioembolism, correlation was moderate using linear mixed models but not significantly different from zero for profile scoring. Joint meta-analysis of LAA and SVD identified strong association (P=1x10⁻⁷) for single nucleotide polymorphisms near the opioid receptor μ1 (OPRM1) gene. Conclusions: Our results suggest that LAA and SVD, which have been hitherto treated as genetically distinct, may share a substantial genetic component. Combined analyses of LAA and SVD may increase power to identify small-effect alleles influencing shared pathophysiological processes.]]> Sat 24 Mar 2018 07:29:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22227 Sat 24 Mar 2018 07:17:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24131 In vitro clotting times were then used to calculate the effective concentration (EC₅₀) in each plasma for four snake venoms with different procoagulant toxins: Pseudonaja textilis, Daboia russelli, Echis carinatus and Calloselasma rhodostoma. Results: Compared to human, PT and aPTT were similar for rat, rabbit and pig, but double for cat and cow, while Guinea pig had similar aPTT but double PT. Fibrinogen and D-dimer levels were similar for all species. Human and rabbit plasmas had the lowest EC₅₀ for P. textilis (0.1 and 0.4 µg/ml), D. russelli (0.4 and 0.1 µg/ml), E. carinatus (0.6 and 0.1 µg/ml) venoms respectively, while cat plasma had the lowest EC₅₀ for C. rhodostoma (11 µg/ml) venom. Cow, rat, pig and Guinea pig plasmas were highly resistant to all four venoms with EC₅₀ 10-fold that of human. Conclusions: Different animal plasmas have varying susceptibility to procoagulant venoms, and excepting rabbits, animal models are not appropriate to test procoagulant activity. In vitro assays on human plasma should instead be adopted for this purpose.]]> Sat 24 Mar 2018 07:16:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22827 Sat 24 Mar 2018 07:16:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24678 in vivo and to determine the underlying mechanism by which simvastatin reduces hepatic steatosis.]]> Sat 24 Mar 2018 07:10:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47489 Mon 23 Jan 2023 11:47:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51777 Mon 18 Sep 2023 15:11:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50970 Mon 14 Aug 2023 15:19:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39586 in silico using the Kaplan-Meier Plotter (n=3,935), the TCGA invasive breast carcinoma (n=960) and GOBO (n=821) data sets. Functional effects of BAALC expression on breast cancer proliferation, migration and invasion were determined in vitro. We demonstrate herein that BAALC expression is progressively increased in primary and breast cancer metastases when compared to normal breast tissue. Increased BAALC mRNA is associated with a reduction in DMFS and disease-free survival, but not OS, in breast cancer patients, even when corrected for tumor grade. We show that overexpression of BAALC in MCF-7 breast cancer cells increases the proliferation, anchorage-independent growth, invasion, and migration capacity of these cells. Conversely, siRNA knockdown of BAALC expression in Hs578T breast cancer cells decreases proliferation, invasion and migration. We identify that this BAALC associated migration and invasion is mediated by focal adhesion kinase (FAK)-dependent signaling and is accompanied by an increase in matrix metalloproteinase (MMP)-9 but not MMP-2 activity in vitro. Our data demonstrate a novel function for BAALC in the control of breast cancer metastasis, offering a potential target for the generation of anti-cancer drugs to prevent breast cancer metastasis.]]> Mon 08 Aug 2022 11:48:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41224 Fri 29 Jul 2022 10:25:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51695 Fri 15 Sep 2023 09:43:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18589 Fri 13 Jul 2018 15:49:03 AEST ]]>