https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45104 Wed 26 Oct 2022 13:16:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29970 Wed 24 Nov 2021 15:50:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43005 Wed 20 Sep 2023 14:36:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23944 Wed 17 Nov 2021 16:32:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29578 Wed 17 Nov 2021 16:29:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24377 1.5 fold in subjects with asthma, whereas, in healthy controls, only 14 entities were differentially expressed. Of the 168 genes that were changed in asthma, several biological processes were overrepresented, with 25 genes involved in "immune system processes". qPCR confirmed that S100P, S100A16, MAL and MUC1 were significantly increased in the asthma group post-meal. We also observed a strong correlation and a moderate correlation between the change in NLRP12 and S100A16 gene expression at 4 h compared to baseline, and the change in total and saturated non-esterified plasma fatty acid levels at 2 h compared to baseline. In summary, our data identifies differences in inflammatory gene expression that may contribute to increased airway neutrophilia following a high fat meal in subjects with asthma and may provide useful therapeutic targets for immunomodulation. This may be particularly relevant to obese asthmatics, who are habitually consuming diets with a high fat content.]]> Wed 17 Nov 2021 16:29:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24832 Wed 15 Dec 2021 16:10:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38201 Wed 11 Aug 2021 10:05:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24171 Wed 11 Apr 2018 17:17:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15270 Wed 11 Apr 2018 16:33:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22005 haemophilus influenzae and pharmacological inhibition in mouse and human macrophages augments phagocytosis, the production of reactive oxygen species, and microbicidal activity. Moreover, inhibition of miR-328 in respiratory models of infection, steroid-induced immunosuppression, and smoke-induced emphysema enhances bacterial clearance. Thus, miRNA pathways can be targeted in the lung to enhance host defence against a clinically relevant microbial infection and offer a potential new anti-microbial approach for the treatment of respiratory diseases.]]> Wed 11 Apr 2018 16:14:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17077 863 =1.31, P =.19). At 1-month follow-up, 93 participants were categorized as matched and 195 as mismatched. They preferred text mode (493/803, 61.4%) over combined (216/803, 26.9%) and video modes (94/803, 11.7%). After the intervention, 20% (26/132) of matched-group participants and 34% (96/282) in the mismatched group changed their delivery mode preference. Time effects were significant for all physical activity outcomes (total physical activity: F_2,801 = 5.07, P = .009; number of activity sessions: F_2,801 = 7.52, P < .001; walking: F_2,801 = 8.32, P < .001; moderate physical activity: F_2,801 = 9.53, P < .001; and vigorous physical activity: F_2,801 = 6.04, P = .002), indicating that physical activity increased over time for both matched and mismatched groups. Matched-group participants improved physical activity outcomes slightly more than those in the mismatched group, but interaction effects were not significant. Physical activity advice acceptability (content scale: t₃₆₈ = .10, P = .92; layout scale: t₃₆₈ = 1.53, P = .12) and website usability (layout scale: t₄₂₆ = .05, P = .96; ease of use scale: t₄₂₆ = .21, P = .83) were generally high and did not differ between the matched and mismatched groups. The only significant difference (t₆₂₁ = 2.16, P = .03) was in relation to total time spent on the website: the mismatched group spent significantly more time on the website (14.4 minutes) than the matched group (12.1 minutes). Conclusion: Participants’ preference regarding delivery mode may not significantly influence intervention outcomes. Consequently, allowing participants to choose their preferred delivery mode may not increase effectiveness of Web-based interventions.]]> Wed 11 Apr 2018 15:23:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20221 Wed 11 Apr 2018 15:04:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14804 Wed 11 Apr 2018 14:46:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19670 Wed 11 Apr 2018 12:43:57 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15553 Wed 11 Apr 2018 11:33:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13786 Wed 11 Apr 2018 11:25:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21737 16 h). Analysis of lncRNA features revealed that intergenic and cis-antisense RNAs are more stable than those derived from introns, as are spliced lncRNAs compared to unspliced (single exon) transcripts. Subcellular localization of lncRNAs indicated widespread trafficking to different cellular locations, with nuclear-localized lncRNAs more likely to be unstable. Surprisingly, one of the least stable lncRNAs is the well-characterized paraspeckle RNA Neat1, suggesting Neat1 instability contributes to the dynamic nature of this subnuclear domain. We have created an online interactive resource (http://stability.matticklab.com) that allows easy navigation of lncRNA and mRNA stability profiles and provides a comprehensive annotation of ∼7200 mouse lncRNAs.]]> Wed 11 Apr 2018 11:06:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15190 Wed 11 Apr 2018 11:02:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15547 Wed 11 Apr 2018 10:43:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14544 Wed 11 Apr 2018 10:15:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18363 Wed 11 Apr 2018 10:06:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24375 Wed 10 Nov 2021 15:05:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30677 p-values = 0.0326, FDR corrected) and an ROC analysis yielding an AUC of 0.87. Crucially, a GP regression revealed that MMN predicted global assessment of functioning (GAF) scores (correlation = 0.73, R² = 0.53, p = 0.0006).]]> Wed 10 Nov 2021 15:05:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28108 Wed 10 Nov 2021 15:04:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30512 Wed 02 Oct 2019 10:14:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31043 Tue 24 Jul 2018 10:12:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13823 Tue 24 Aug 2021 14:27:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16097 Tue 24 Aug 2021 14:26:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20160 36-fold reduced activity against rings, suggesting that they can discriminate between helical or ring oligomerization states. 4a and 6a inhibited dynamin-dependent endocytosis of transferrin in multiple cell types (IC50 of 5.7 and 5.8 μM, respectively), at least sixfold more potently than dynasore, but had no effect on dynamin-independent endocytosis of cholera toxin. 4a also reduced synaptic vesicle endocytosis and activity-dependent bulk endocytosis in cultured neurons and synaptosomes. Overall, 4a and 6a are improved and versatile helical dynamin and endocytosis inhibitors in terms of potency, non-specific binding and cytotoxicity. The data further suggest that the ring oligomerization state of dynamin is not required for clathrin-mediated endocytosis.]]> Tue 24 Aug 2021 14:23:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38873 Bacteroides species and describe the antimicrobial resistance biogeography along the intestine. We also detail which species, at which locations, are involved with the tryptophan/indole pathway, whose malfunctioning has been linked to pathologies including inflammatory bowel disease. Our study thus provides invaluable resources for investigating mechanisms connecting gut microbiota and host pathophysiology.]]> Tue 22 Feb 2022 16:36:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27769 SNP]) and tested the hypothesis that WMH heritability differs between hypertensive and nonhypertensive individuals. Methods: WMHV was measured on MRI in the stroke-free cerebral hemisphere of 2336 ischemic stroke cases with GWAS data. After adjustment for age and intracranial volume, we determined which cardiovascular risk factors were independent predictors of WMHV. Using the genome-wide complex trait analysis tool to estimate H_SNP for WMHV overall and within subgroups stratified by risk factors found to be significant in multivariate analyses. Results: A significant proportion of the variance of WMHV was attributable to common SNPs after adjustment for significant risk factors (H_SNP=0.23; P=0.0026). H_SNP estimates were higher among hypertensive individuals (H_SNP=0.45; P=7.99x10^-5); this increase was greater than expected by chance (P=0.012). In contrast, estimates were lower, and nonsignificant, in nonhypertensive individuals (H_SNP=0.13; P=0.13). Conclusions: A quarter of variance is attributable to common SNPs, but this estimate was greater in hypertensive individuals. These findings suggest that the genetic architecture of WMH in ischemic stroke differs between hypertensives and nonhypertensives. Future WMHV GWAS studies may gain power by accounting for this interaction.]]> Tue 21 Jul 2020 09:44:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45060 Tue 14 Nov 2023 14:40:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25796 Tue 11 Feb 2020 09:19:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39116 Tue 10 May 2022 15:01:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30493 2; odds ratio, 2.710; P=0.040). No difference was found in reperfusion rate after treatment between patients with and without SMCV-(P > 0.05). In patients achieving major reperfusion (=80%), there was no difference in 24-hour infarct volume, or rate of poor outcome between patients with and without SMCV-(P > 0.05). However, in those without major reperfusion, patients with SMCV-had larger 24-hour infarct volume (P=0.011), higher rate of poor outcome (P=0.012), and death (P=0.032) compared with those with SMCV filling. SMCV-was significantly associated with brain edema at 24 hours (P=0.037), which, in turn, was associated with poor 3-month outcome (P=0.002). Conclusions: Lack of SMCV filling contributed to poor outcome after thrombolysis, especially when reperfusion was not achieved. The main deleterious effect of poor venous filling appears related to the development of brain edema.]]> Thu 28 Oct 2021 13:03:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41194 Thu 28 Jul 2022 11:12:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24812 Thu 14 Apr 2022 11:00:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40631 Thu 11 Aug 2022 09:02:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47845 Thu 02 Feb 2023 15:50:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31553 Sat 24 Mar 2018 08:44:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31532 Sat 24 Mar 2018 08:43:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14868 Sat 24 Mar 2018 08:21:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20213 Sat 24 Mar 2018 08:06:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20947 50, p=4.02E-06), which may have clinical/biological implications.]]> Sat 24 Mar 2018 08:06:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20786 Sat 24 Mar 2018 08:06:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20838 Sat 24 Mar 2018 08:05:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19034 Sat 24 Mar 2018 08:05:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19924 Sat 24 Mar 2018 08:03:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21475 Sat 24 Mar 2018 08:03:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19456 Sat 24 Mar 2018 08:02:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18965 Sat 24 Mar 2018 07:58:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16896 Sat 24 Mar 2018 07:58:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19958 Sat 24 Mar 2018 07:58:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20869 Sat 24 Mar 2018 07:57:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20890 Sat 24 Mar 2018 07:57:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17922 Sat 24 Mar 2018 07:56:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17878 Sat 24 Mar 2018 07:56:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19115 Sat 24 Mar 2018 07:55:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20582 Sat 24 Mar 2018 07:55:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21757 Sat 24 Mar 2018 07:53:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20171 Sat 24 Mar 2018 07:51:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20159 Sat 24 Mar 2018 07:51:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20196 Sat 24 Mar 2018 07:51:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18773 trend= 0.086). Conclusion: Seasonal fluctuation of MS births as found in this worldwide cohort of patients with MS did not correlate with variation in seasonal fluctuation of UV-light. Most likely, it results from a complex interplay between fluctuation of sunlight, behavioural factors, other environmental factors and (epi)genetic factors.]]> Sat 24 Mar 2018 07:51:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26605 Sat 24 Mar 2018 07:33:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26609 Sat 24 Mar 2018 07:33:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27228 Sat 24 Mar 2018 07:32:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27256 Sat 24 Mar 2018 07:29:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25904 Sat 24 Mar 2018 07:27:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28305 97%) to plasma proteins, there is the strong possibility that co-administered CF drugs may compete for the same plasma protein binding sites and impact the free drug concentration. This, in turn, could lead to drastic changes in the in vivo efficacy of ivacaftor and therapeutic outcomes. This biochemical study compares the binding affinity of ivacaftor and co-administered CF drugs for human serum albumin (HSA) and α₁-acid glycoprotein (AGP) using surface plasmon resonance and fluorimetric binding assays that measure the displacement of site-selective probes. Because of their ability to strongly compete for the ivacaftor binding sites on HSA and AGP, drug–drug interactions between ivacaftor are to be expected with ducosate, montelukast, ibuprofen, dicloxacillin, omeprazole, and loratadine. The significance of these plasma protein drug–drug interactions is also interpreted in terms of molecular docking simulations. This in vitro study provides valuable insights into the plasma protein drug–drug interactions of ivacaftor with co-administered CF drugs. The data may prove useful in future clinical trials for a staggered treatment that aims to maximize the effective free drug concentration and clinical efficacy of ivacaftor.]]> Sat 24 Mar 2018 07:27:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26551 Sat 24 Mar 2018 07:26:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30253 Sat 24 Mar 2018 07:24:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22192 Sat 24 Mar 2018 07:16:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23404 IIbß₃, irreversible platelet aggregation and thrombus stabilisation. Tetraspanin superfamily member CD151 associates with integrin a_IIbß₃ and plays critical roles in regulation of thrombus growth and stability in vivo. The possible functional relationship between P2Y₁₂ and CD151 in a molecular cluster in platelets may affect thrombus formation. Hence our aim was to investigate the physical and functional requirements for this association in platelets. Our investigations reveal a specific and constitutive association between CD151 and P2Y₁₂ receptor in human platelets shown by immunoprecipitation/western blot studies and by flow cytometry. Specifically, the prominent association involves CD151 with P2Y₁₂ oligomers, and to a lesser extent P2Y₁₂ monomers. This association is not altered by platelet aggregation induced by different agonists. There is also a distinct complex of tetraspanin CD151 with ADP purinergic receptor P2Y₁₂ but not P2Y₁. P2Y₁₂ oligomer interaction with CD151 is selective as compared to other tetraspanins. To investigate the functional relationship between these receptors in platelets we used wild-type or CD151 knockout (KO) mice treated with either PBS or 50 mg/kg clopidogrel. CD151 KO mice treated with clopidogrel exhibited synergy in delayed kinetics of clot retraction, in PAR-4 and collagen-mediated platelet aggregation, platelet spreading on fibrinogen and without restricting cAMP inhibition. Clopidogrel treated CD151 KO arterioles showed smaller and less stable thrombi with increased tendency to embolise ex vivo and in vivo. These studies demonstrate a complementary role between CD151 and P2Y₁₂ receptor in platelets in regulating thrombus growth and stability.]]> Sat 24 Mar 2018 07:13:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23405 Sat 24 Mar 2018 07:13:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22118 Sat 24 Mar 2018 07:13:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23578 −4). In a replication phase, we combined these data with previous genome-wide association study (GWAS) data from an independent 14,802 subjects with multiple sclerosis and 26,703 healthy controls. In these 80,094 individuals of European ancestry, we identified 48 new susceptibility variants (P < 5.0 x 10⁻⁸), 3 of which we found after conditioning on previously identified variants. Thus, there are now 110 established multiple sclerosis risk variants at 103 discrete loci outside of the major histocompatibility complex. With high-resolution Bayesian fine mapping, we identified five regions where one variant accounted for more than 50% of the posterior probability of association. This study enhances the catalog of multiple sclerosis risk variants and illustrates the value of fine mapping in the resolution of GWAS signals.]]> Sat 24 Mar 2018 07:12:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22677 Sat 24 Mar 2018 07:12:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22107 Sat 24 Mar 2018 07:10:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24170 Sat 24 Mar 2018 07:09:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45522 Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa. The combination of polymyxin B and sertraline showed synergistic antibacterial activity in checkerboard and static time-kill assays at clinically relevant concentrations against both polymyxin-susceptible and polymyxin-resistant isolates. The potential antimicrobial mode of action of the combination was investigated against P.aeruginosa FADDI-PA024 using untargeted metabolomics alongside scanning and transmission electron microscopy (EM). Scanning and transmission EM revealed that the polymyxin B and sertraline combination resulted in greater damage to the bacterial cell compared to each drug alone. Metabolomics results showed that the combination significantly affected the bacterial ability to remodel its outer membrane. This was reflected by the major perturbation of glycerophospholipids and fatty acids and the pantothenate and coenzyme A (CoA) pathways, which feed fatty acid elongation (e.g., trans-hexadec-2-enoyl-CoA) as well as inhibit the biosynthesis of lipopolysaccharide and peptidoglycan. The combination also inhibited the polymyxin resistance phosphoethanolamine (pEtN) lipid A modification pathway, indicated by the declined levels of phosphoethanolamine. In summary, the present study highlights the potential possibilities of a polymyxin-sertraline combination for the treatment of infections caused by multidrug resistant Gram-negative bacteria such as central nervous system (CNS) infections via direct intraventricular/intrathecal delivery.]]> Mon 31 Oct 2022 14:09:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24046 Mon 23 Sep 2019 14:04:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31959 Mon 23 Sep 2019 11:55:41 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39176 P <.05. Results: Older respondents and females reported higher levels of both cooking and food skills confidence compared to younger and male participants, all P <.001. Cooking and food skills confidence scores were highly correlated (r =.70, P <.001), but weakly correlated with ARFS (r =.22, P <.001; r =.31, P <.001, respectively). Participants with higher diet quality scores had greater cooking and food skills confidence and they consumed less takeaway food (P <.001 and P =.006, respectively). Sixteen percent of the variance in ARFS was accounted for, with age, sex, food creativity and food skills confidence contributing the most variability. Conclusions: Strategies to improve food skills confidence could potentially enhance diet quality and variety to a greater degree than focusing on cooking skills alone. However, development of both skills sets should be encouraged within education programs and targeted to differing aspects of diet quality. Tailoring interventions to specific population groups with low confidence in their skills, including younger adults and males, may facilitate individuals in making healthy food choices.]]> Mon 23 May 2022 14:54:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39174 n = 65 indices). Some indices were age specific: infant (< 24-months; n = 8 indices), child (2–12-years; n = 16), adolescent (13–18 years; n = 8), and child/adolescent (n = 14). Thirty-seven indices evaluated for validity and/or reliability. Eleven of the 15 indices which investigated associations with prospective health outcomes reported significant results, such as improved IQ, quality of life, blood pressure, body composition, and prevalence of metabolic syndrome. Conclusions: Research utilising diet quality indices in paediatric populations is rapidly expanding internationally. However, few indices have been evaluated for validity, reliability, or association with health outcomes. Further research is needed to determine the validity, reliability, and association with health of frequently utilised diet quality indices to ensure data generated by an index is useful, applicable, and relevant. Registration: PROSPERO number: CRD42018107630.]]> Mon 23 May 2022 14:38:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39754 Mon 20 Jun 2022 12:01:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20652 Mon 14 Dec 2020 14:04:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42239 Fri 26 Aug 2022 09:43:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46439 Fri 25 Nov 2022 15:28:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46436 Fri 25 Nov 2022 12:43:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31243 Fri 24 Aug 2018 09:05:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39946 p = 0.04) compared with those with a trade, vocational or university-level education. Just over one-third of a sample of Australian cancer patients were not asked about all assessed lifestyle risk factors following their diagnosis of cancer. These findings suggest there is scope to improve identification of lifestyle risk factors among cancer survivors.]]> Fri 22 Jul 2022 11:44:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39704 Fri 17 Jun 2022 16:56:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44399 Fri 14 Oct 2022 08:48:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47366 Fri 13 Jan 2023 14:57:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47286 Fri 13 Jan 2023 10:24:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30102 Fri 11 Jun 2021 13:30:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25061 80 %. Culture in serum-free conditions selected for growth of normal renal proximal tubule epithelial cells. Transcriptional profiling of ccRCC and matched normal cell cultures identified up- and down-regulated networks in ccRCC and comparison to The Cancer Genome Atlas confirmed the clinical validity of our cell cultures. Conclusions: The ability to establish primary cultures of ccRCC cells and matched normal kidney epithelial cells from almost every patient provides a resource for future development of novel therapies and personalized medicine for ccRCC patients.]]> Fri 03 Dec 2021 10:33:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24090 Aspergillus fumigatus allergen mouse model of EoE. Because IL-33 induction was transient in this model and chronicity of IL-33 expression has been demonstrated in humans, naive mice were treated with recombinant IL-33 for 1 wk and esophageal pathology was evaluated. IL-33 application produced changes consistent with phenotypically early EoE, including transmural eosinophilia, mucosal hyperproliferation, and upregulation of eosinophilic genes and chemokines. Th2 cytokines, including IL-13, along with innate lymphoid cell group 2, Th1/17, and M2 macrophage marker genes, were increased after IL-33 application. IL-33-induced eosinophilia was ablated in IL-13 null mice. In addition, IL-33 induced a profound inhibition of the regulatory T cell gene signature. We conclude that IL-33 gene expression is associated with pediatric EoE development and that application of recombinant protein in mice phenocopies the early clinical phase of the human disease in an IL-13-dependent manner. IL-33 inhibition of esophageal regulatory T cell function may induce loss of antigenic tolerance, thereby providing a mechanistic rationale for EoE development.]]> Fri 03 Dec 2021 10:32:37 AEDT ]]>